ORIGINAL_ARTICLE
Traditional Persian topical medications for gastrointestinal diseases
Drug delivery across the skin is used for several millennia to ease gastrointestinal (GI) ailments in Traditional Persian Medicine (TPM). TPM topical remedies are generally being applied on the stomach, lower abdomen, lower back and liver to alleviate GI illnesses such as dyspepsia, gastritis, GI ulcers, inflammatory bowel disease, intestinal worms and infections. The aim of the present study is to survey the topical GI remedies and plant species used as ingredients for these remedies in TPM. In addition, pharmacological activities of the mentioned plants have been discussed. For this, we searched major TPM textbooks to find plants used to cure GI problems in topical use. Additionally, scientific databases were searched to obtain pharmacological data supporting the use of TPM plants in GI diseases. Rosa × damascena, Pistacia lentiscus, Malus domestica, Olea europaea and Artemisia absinthium are among the most frequently mentioned ingredients of TPM remedies. β-asarone, amygdalin, boswellic acids, guggulsterone, crocin, crocetin, isomasticadienolic acid, and cyclotides are the most important phytochemicals present in TPM plants with GI-protective activities. Pharmacological studies demonstrated GI activities for TPM plants supporting their extensive traditional use. These plants play pivotal role in alleviating GI disorders through exhibiting numerous activities including antispasmodic, anti-ulcer, anti-secretory, anti-colitis, anti-diarrheal, antibacterial and anthelmintic properties. Several mechanisms underlie these activities including the alleviation of oxidative stress, exhibiting cytoprotective activity, down-regulation of the inflammatory cytokines, suppression of the cellular signaling pathways of inflammatory responses, improving re-epithelialization and angiogenesis, down-regulation of anti-angiogenic factors, blocking activity of acetylcholine, etc.
https://ijbms.mums.ac.ir/article_8349_77c61303d63e97c578d7bf84d497a6d0.pdf
2017-03-01
222
241
10.22038/ijbms.2017.8349
Gastrointestinal
Medicinal Plants
Olea europaea
Pistacia lentiscus
Rosa × damascene
Topical delivery
Traditional Medicine
Laleh
Dehghani Tafti
ldehghanitafti@gmail.com
1
Department of History and Civilization of Islamic Nations, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Seyyed Mahyar
Shariatpanahi
mahyar.shariatpanahi@gmail.com
2
Department of History and Civilization of Islamic Nations, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Mahmoud
Mahdavi Damghani
javadi.behjat@yahoo.com
3
Department of History and Civilization of Islamic Nations, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Behjat
Javadi
javadib@mums.ac.ir
4
Department of Traditional Pharmacy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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161. Voravuthikunchai SP, Sririrak T, Limsuwan S, Supawita T, Iida T, Honda T. Inhibitory effects of active compounds from Punica granatum pericarp on verocytotoxin production by enterohemorrhagic Escherichia coli O157: H7. J Health Sci 2005; 51:590-596.
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165. Sadraei H, Asghari G, Emami S. Inhibitory effect of Rosa damascena Mill flower essential oil, geraniol and citronellol on rat ileum contraction. Res Pharm Sci 2013; 8:17-23.
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166. Latifi G, Ghannadi A, Minaiyan M. Anti-inflammatory effect of volatile oil and hydroalcoholic extract of Rosa damascena Mill. on acetic acid-induced colitis in rats. Res Pharm Sci 2015; 10:514-522.
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167. Janbaz KH, Shabbir A, Mehmood MH, Gilani AH. Pharmacological basis for the medicinal use of Rhus coriaria in hyperactive gut disorders. Bangladesh J. Pharmacol 2014; 9:636-644.
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176
177. Pandian RS, Anuradha CV, Viswanathan P. Gastroprotective effect of fenugreek seeds (Trigonella foenum graecum) on experimental gastric ulcer in rats. J Ethnopharmacol 2002; 81:393-397.
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181
ORIGINAL_ARTICLE
Anti-melanogenic activity of Viola odorata different extracts on B16F10 murine melanoma cells
Objective(s): In previous studies, antioxidant activity of Viola odorata L. has been demonstrated. In this study, we have investigated the anti-melanogenic effect of extract and fractions of the plant in B16F10 cell line. Materials and Methods: Impact of different increasing concentrations of extract and fractions of V. odorata was evaluated on cell viability, cellular tyrosinase, melanin content and mushroom tyrosinase as well as ROS production in B16F10 murine melanoma cell line. Results: Viola odorata had no cytotoxicity on B16F10 cells compared to control group. Kojic acid as positive control had significant decreasing effects on cellular and mushroom tyrosinase activity, melanin content and ROS production (P<0.001, for all cases). V. odorata (1-20 µg/ml) decreased all measured parameters including cellular tyrosinase and melanin content as well as ROS production and among all extract and fractions ethyl acetate fraction had the best effect (P<0.05). Conclusion: Viola odorata had promising anti-melanogenic activity through inhibition of cellular tyrosinase activity and ROS production as well as melanin content. More basic and clinical studies need to aver its impact.
https://ijbms.mums.ac.ir/article_8350_e6a4929429de3c380608dcb8ec0316d7.pdf
2017-03-01
242
249
10.22038/ijbms.2017.8350
B16F10 cell line
Melanin
ROS
Tyrosinase
Violaceae
Viola odorata L
Vafa
Baradaran Rahimi
baradaranv941@mums.ac.ir
1
Student Research Committee, Department of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Vahid Reza
Askari
vahidrezaaskari
2
Student Research Committee, Department of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Ahmad
Emami
saemami@mums.ac.ir
3
Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zahra
Tayarani-Najaran
tayraninz@mums.ac.ir
4
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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18. Cestari TF, Dantas LP, and Boza JC. Acquired hyperpigmentations.An Bras Dermatol 2014; 1: 11-25.
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19. Sadraei H, Asghari G, and Emami S. Effect of Rosa damascena Mill. flower extract on rat ileum.Res Pharm Sci 2013; 4: 277-284.
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42
ORIGINAL_ARTICLE
Association between the synonymous variant organic cation transporter 3 (OCT3)-1233G>A and the glycemic response following metformin therapy in patients with type 2 diabetes
Objective(s): Organic cation transporter 3 (OCT3) as a high-capacity transporter contribute to the metabolism of metformin. The present study was conducted to determine the genotype frequencies of the variant OCT3-1233G>A (rs2292334) in patients with newly diagnosed type 2 diabetes (T2D) and its relationship with response to metformin. Materials and Methods: This study included 150 patients with T2D who were classified into two groups following three months of metformin therapy: responders (by more than 1% reduction in HbA1c from baseline) and nonresponders (less than 1% reduction in HbA1c from baseline). PCR-based restriction fragment length polymorphism (RFLP) served to genotype OCT3-564G>A variant. Results: The parameters such as HbA1c (P<0.001) and BMI (P<0.001) in both patients with GA + AA genotype and GG genotype decreased significantly following 3 months of metformin therapy compared with baseline. The mean reduction in HbA1c levels following 3 months was higher in patients with the A allele (0.77% reduction from baseline) than in those with the homozygous G allele (0.54% reduction from baseline). Also, in GA + AA genotypes compared with GG genotypes, the mean reduction in HbA1c values from baseline was 0.34% for responders and 0.14% for non-responders. Conclusion: Considering the roles of genetic variations in the function of metformin transporters, the effect of variations such as 1233G>A in the OCT3, which is a high-capacity transporter widely expressed in various tissues cannot be ignored. Comparing the allele frequencies of OCT3-1233G>A variant in our study and different ethnic populations confirm that the variant is a highly polymorphic variant.
https://ijbms.mums.ac.ir/article_8351_51843a2165756fe5d34ad1b86bbae345.pdf
2017-03-01
250
255
10.22038/ijbms.2017.8351
HbA1c
Metformin
OCT3
Organic cation transporter 3
Type 2 diabetes
Seyyedeh Raheleh
Hosseyni-Talei
srht.hosseini@gmail.com
1
Immunogenetic Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Abdolkarim
Mahrooz
kmahrooz2@gmail.com
2
Immunogenetic Research Center, Mazandaran University of Medical Sciences, Sari, Iran
LEAD_AUTHOR
Mohammad Bagher
Hashemi-Soteh
3
Immunogenetic Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Maryam
Ghaffari-Cherati
mghafaricherati@gmail.com
4
Immunogenetic Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Ahad
Alizadeh
st.alizadeh@gmail.com
5
Department of Epidemiology and Reproductive Health, Reproductive Epidemiology Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
AUTHOR
1.Weber MB, Narayan KV. Preventing type 2 diabetes: genes or lifestyle? Prim Care Diabetes 2008; 2:65–66.
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2.Holstein A, Seeringer A, Kovacs P. Therapy with oral antidiabetic drugs: applied pharmacogenetics. Br J Diabetes Vasc Dis 2001; 11:10–16.
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3.Goldenberg R, Punthakee Z. Definition, classification and diagnosis of diabetes, prediabetes and metabolic syndrome. Can J Diabetes 2013; 37; S8–S11.
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4.Avery P, Mousa SS, Mousa SA. Pharmacogenomics in type II diabetes mellitus management: steps toward personalized medicine. Pharmgenomics Pers Med 2009; 2:79–91.
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5.Standards of medical care in diabetes-2009. Diabet Care 2009; 32: S13–S61.
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6.Mahrooz A, Parsanasab H, Hashemi-Soteh MB, Kashi Z, Bahar A, Alizadeh A, Mozayeni M. The role of clinical response to metformin in patients newly diagnosed with type 2 diabetes: a monotherapy study. Clin Exp Med 2015; 15: 159–165.
6
7.Kashi Z, Mahrooz A, Kianmehr A, Alizadeh A. The role of metformin response in lipid metabolism in patients with recent‑onset type 2 diabetes: HbA1c level as a criterion for designating patients as responders or nonresponders to metformin. PLoS One 2016; 11:e0151543.
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8.Pacanowski MA, Hopley CW, Aquilante CL. Interindividual variability in oral antidiabetic drug disposition and response: the role of drug transporter polymorphisms. Expert Opin Drug MetabToxicol 2008; 4:529–544.
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9.Gong Li, GoswamiSrijib, Giacomini KM, Altman RB, Klein TE. Metformin pathways: pharmacokinetics and pharmacodynamics. Pharmacogenet Genomics 2012; 22:820–827.
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10.Marchetti P, Scharp DW, Giannarelli R, Benzi L, Cicchetti P, Ciccarone AM, et al. Metformin potentiates glucose-stimulated insulin secretion. Diabet Care 1996; 19:781–782.
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11.Robert F, Fendri S, Hary L, Lacroix C, Andréjak M, Lalau JD. Kinetics of plasma and erythrocyte metformin after acute administration in healthy subjects. Diabet Metab 2003; 29:279–283.
11
12.Kashi Z, Masoumi P, Mahrooz A, Hashemi-Soteh MB, Bahar A, Alizadeh A. The variant organic cation transporter 2 (OCT2)-T201M contribute to changes in insulin resistance in patients with type 2 diabetes treated with metformin. Diabetes Res Clin Pract 2015; 108:78–83.
12
13.Wu X, Huang W, Ganapathy ME, Wang H, Kekuda R, Conway SJ, et al. Structure, function, and regional distribution of the organic cation transporter OCT3 in the kidney. Am J Physiol Renal Physiol 2000; 279:F449–458.
13
14.Chen L, Pawlikowski B, Schlessinger A, More SS, Stryke D, Johns SJ, et al. Role of organic cation transporter 3 (SLC22A3) and its missense variants in the pharmacologic action of metformin. Pharmacogenet Genomics 2010; 20:687–699.
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15.Kerb R. Implications of genetic polymorphisms in drug transporters for pharmacotherapy. Cancer Lett 2006; 234:4–33.
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16.Lazar A, Grundemann D, Berkels R, Taubert D, Zimmermann T, Schömig E. Genetic variability of the extraneuronal monoamine transporter EMT (SLC22A3). J Hum Genet 2003; 48: 226-230.
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17.Aoyama N, Takahashi N, Kitaichi K, Ishihara R, Saito S, Maeno N, et al. Association between gene polymorphisms of SLC22A3 and methamphetamine use disorder. Alcohol Clin Exp Res 2006; 30:1644–1649.
17
18.Todd JN, Florez JC. An update on the pharmacogenomics of metformin: progress, problems and potential. Pharmacogenomics 2014; 15:529–539.
18
19.Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972; 18:499–502.
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20.Hengen N, Lizer MH, Kidd RS. Evaluation of genetic variations in organic cationic transporter 3 in depressed and nondepressed subjects. ISRN Pharmacol 2011; 2011:161740.
20
21.Takane H, Shikata E, Otsubo K, Higuchi S, Ieiri I, et al. Polymorphism in human organic cation transporters and metformin action. Pharmacogenomics 2008; 9:415–422.
21
22.Becker ML, Visser LE, Van Schaik RH, Hofman A, Uitterlinden AG, Stricker BH. Genetic variation in the organic cation transporter 1 is associated with metformin response in patients with diabetes mellitus. Pharmacogenomics J 2009; 9:242–247.
22
23.Nies AT, Koepsell H, Winter S, Burk O, Klein K, Kerb R, et al. Expression of organiccation transporters OCT1 (SLC22A1) and OCT3 (SLC22A3) is affected by genetic factors and cholestasis in human liver. Hepatology 2009; 50:1227–1240.
23
24.Tzvetkov MV, Vormfelde SV, Balen D, Meineke I, Schmidt T, Sehrt D, et al. The effects of genetic polymorphisms in the organic cation transporters OCT1, OCT2, and OCT3 on the renal clearance of metformin. Clin Pharmacol Ther 2009; 86:299–306.
24
25.Wallace TM, Matthews DR. The assessment of insulin resistance in man. Diabet Med 2002; 19:527–534.
25
26.Rena G, Pearson ER, Sakamoto K. Molecular mechanism of action of metformin: old or new insights? Diabetologia 2013; 56:1898–1906.
26
27.Bosi E. Metformin – the gold standard in type 2 diabetes: what does the evidence tell us? Diabetes Obes Metab 2009; 11:3–8.
27
28.Abdul-Ghani MA, Puckett C, Triplitt C, Maggs D, Adams J, Cersosimo E, et al. Initial combination therapy with metformin, pioglitazone and exenatide is more effective than sequential add-on therapy in subjects with new-onset diabetes. Results from the efficacy and durability of initial combination therapy for type 2 Diabetes (EDICT): a randomized trial. Diabetes Obes metab 2015; 17:268–275.
28
ORIGINAL_ARTICLE
Injury to skeletal muscle of mice following acute and sub-acute pregabalin exposure
Objective(s): Pregabalin (PGB) is a new antiepileptic drug that has received FDA approval for patient who suffers from central neuropathic pain, partial seizures, generalized anxiety disorder, fibromyalgia and sleep disorders. This study was undertaken to evaluate the possible adverse effects of PGB on the muscular system of mice. Materials and Methods: To evaluate the effect of PGB on skeletal muscle, the animals were exposed to a single dose of 1, 2 or 5 g /kg or daily doses of 20, 40 or 80 mg/kg for 21 days, intraperitoneally (IP). Twaenty-four hr after the last drug administration, all animals were sacrificed. The level of fast-twitch skeletal muscle troponin I and CK-MM activity were evaluated in blood as an indicator of muscle injury. Skeletal muscle pathological findings were also reported as scores ranging from 1 to 3 based on the observed lesion. Results: In the acute and sub-acute toxicity assay IP injection of PGB significantly increased the activity and levels of CK-MM and fsTnI compared to the control group. Sub-acute exposure to PGB caused damages that include muscle atrophy, infiltration of inflammatory cells and cell degeneration. Conclusion: PGB administration especially in long term care causes muscle atrophy with infiltration of inflammatory cells and cell degeneration. The fsTnI and CK-MM are reliable markers in PGB-related muscle injury. The exact mechanisms behind the muscular damage are unclear and necessitate further investigations.
https://ijbms.mums.ac.ir/article_8352_6f8deb7a543479eb0b44d34ce3224aa5.pdf
2017-03-01
256
259
10.22038/ijbms.2017.8352
Acute
Muscle injury
Pregabalin
Skeletal muscle
Subacute
Mohammad
Moshiri
moshiri.mo@gmail.com
1
Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Adel
Moallem
samoallem@yahoo.com
2
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Armin
Attaranzadeh
armin.atta@gmail.com
3
Milad Infertility Center, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zahra
Saberi
saberiz2@mums.ac.ir
4
Nanotechnology Research Center School of Pharmacy, Mashhad University Medical Sciences, Mashhad, Iran
AUTHOR
Leila
Etemad
etemadl@mums.ac.ir
5
Pharmaceutical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Etemad L, Moshiri M, Mohammadpour AH, Vahdati Mashhadi N, Moallem SA, Teratogenic effects of pregabalin in mice. Iran J Basic Med Sci 2013; 16: 1065-1070.
1
2. Freynhagen R, Grond S, Schupfer G, Hagebeuker A, Schmelz M, Ziegler D, et al. Efficacy and safety of pregabalin in treatment refractory patients with various neuropathic pain entities in clinical routine. Int J Clin Pract 2007; 61: 1989-1996.
2
3. Sebastian B, Talikoti AT, Nelamangala K, Krishnamurthy D. Effect of oral pregabalin as preemptive analgesic in patients undergoing lower limb orthopedic surgeries under spinal anaesthesia. J Clin Diagn Res 2016; 10: UC01-4.
3
4. Etemad L, Jafarian AH, Moallem SA. Pathogenesis of pregabalin-induced limb defects in mouse embryos. J Pharm Pharm Sci 2015; 18: 882-889.
4
5. Vassallo JD, Janovitz EB, Wescott DM, Chadwick C, Lowe-Krentz LJ, Lehman-McKeeman LD. Biomarkers of drug-induced skeletal muscle injury in the rat: troponin I and myoglobin. Toxicol Sci 2009; 111: 402-412.
5
6. Brazeau GA. Drug induced muscle damage. In: Reznic AZ, Packer L, Sen CK, Holloszy JO, Jackson MJ. editors. Oxidative stress in muscle muscle. 1st ed. Springer Basel AG; 1998.p.295-316.
6
7. Jones JD, Kirsch HL, Wortmann RL, Pillinger MH. The causes of drug-induced muscle toxicity. Curr Opin Rheumatol 2014; 26: 697-703.
7
8. Anonymous, Lyrica Prescribing Information. USA: Pfizer Inc; 2004.
8
9. Sorichter S, Mair J, Koller A, Gebert W, Rama D, Calzolari C, et al. Skeletal troponin I as a marker of exercise-induced muscle damage. J Appl Physiol 1997; 83: 1076-1082.
9
10. Simpson JA, Labugger R, Collier C, Brison RJ, Iscoe S, Van Eyk JE, Fast and slow skeletal troponin I in serum from patients with various skeletal muscle disorders: a pilot study. Clin Chem 2005; 51: 966-972.
10
11. Apple FS, Tissue specificity of cardiac troponin I, cardiac troponin T and creatine kinase-MB. Clin Chim Acta 1999; 284: 151-159.
11
12. Sills GJ, The mechanisms of action of gabapentin and pregabalin. Curr Opin Pharmacol 2006; 6: 108-113.
12
13. Gong HC, Hang J, Kohler W, Li L, Su TZ. Tissue-specific expression and gabapentin-binding properties of calcium channel alpha 2 delta subunit subtypes. J Membr Biol 2001; 184: 35-43.
13
14. Patel R, Dickenson AH, Mechanisms of the gabapentinoids and alpha 2 delta-1 calcium channel subunit in neuropathic pain. Pharmacol Res Perspect 2016; 4: e00205.
14
15. Papadimitriou A, Servidei S. Late onset lipid storage myopathy due to multiple acyl CoA dehydrogenase deficiency triggered by valproate. Neuromuscul Disord 1991; 1: 247-252.
15
16. Silva MF, Aires CC, Luis PB, Ruiter JP, L IJ, Duran M, et al. Valproic acid metabolism and its effects on mitochondrial fatty acid oxidation: a review. J Inherit Metab Dis 2008; 31: 205-216.
16
17. Kaufman MB, Choy M. Pregabalin and simvastatin: first report of a case of rhabdomyolysis. P T 2012; 37: 579-595.
17
ORIGINAL_ARTICLE
The effect of caffeine on orthodontic tooth movement in rats
Objective(s): to determine the effect of different doses of caffeine on orthodontic tooth movement (OTM) in rats. Materials and Methods: Forty male 250-300 g Sprague-Dawley rats were randomly divided into four groups of ten animals each and received 0 (control), 1 g/l, 2 g/l and 3 g/l caffeine in tap water for 3 days. Orthodontic appliances were ligated between the maxillary first molars and incisors on the 4th day of the study period. All rats were sacrificed after 2 weeks of treatment after which OTM was measured. Hematoxylin/eosin-stained sections of the molars were prepared and the mesial roots were examined for resorption-lacunae depth and osteoclast number. ANOVA was used for statistical analysis (P<0.05). Results: A significant decrease in OTM was observed only in the 2 g/l (P=0.043) and 3 g/l (P<0.01) caffeine-receiving rats compared to the control animals. Osteoclast counts and resorption-lacunae depths demonstrated significant differences between each of the caffeine groups and control rats (P<0.05). None of the variables showed significant differences between the caffeine groups (P>0.05). Conclusion: According to our findings, one of the effects of caffeine consumption during orthodontic treatment in rats was decreased root resorption. Additionally, concentrations of 2 g/l and 3 g/l inhibited OTM which seems to be due to its influence on osteoclast numbers.
https://ijbms.mums.ac.ir/article_8353_d3284eb83e5a352fc2bf27a848c8a1f8.pdf
2017-03-01
260
264
10.22038/ijbms.2017.8353
Caffeine
Rats
root resorption
Tooth movement
Mohsen
Shirazi
mohsenshirazi8@yahoo.com
1
Dental Research Center, Dentistry Research Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Hamed
Vaziri
hamedvaziriii@gmail.com
2
Private practice, Houston, Texas
AUTHOR
Behzad
Salari
b.salarii@gmail.com
3
Orthodontic Resident, Department of Orthodontics, School of Dentistry, Qazvin University of Medical Sciences, Qazvin, Iran
AUTHOR
Pouria
Motahhari
pouriamotahhariii@yahoo.com
4
Department of Oral and Maxillofacial Pathology, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shahroo
Etemad-Moghadam
shahrooetemad@yahoo.com
5
Dental Research Center, Dentistry Research Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ahmad Reza
Dehpour
dehpoura@sina.tums.ac.ir
6
Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Meikle MC. The tissue, cellular, and molecular regulation of orthodontic tooth movement: 100 years after Carl Sandstedt. Eur J Orthod 2006; 28:221-240.
1
2. Shirazi M, Dehpour AR, Jafari F. The effect of thyroid hormone on orthodontic tooth movement in rats. J Clin Pediatr Dent 1999; 23:259-264.
2
3. Li F, Li G, Hu H, Liu R, Chen J, Zou S. Effect of parathyroid hormone on experimental tooth movement in rats. Am J Orthod Dentofacial Orthop 2013; 144:523-532.
3
4. Kawakami M, Takano-Yamamoto T. Local injection of 1,25-dihydroxyvitamin D3 enhanced bone formation for tooth stabilization after experimental tooth movement in rats. J Bone Miner Metab 2004; 22:541-546.
4
5. Shirazi M, Nilforoushan D, Alghasi H, Dehpour AR. The role of nitric oxide in orthodontic tooth movement in rats. Angle Orthod 2002; 72:211-215.
5
6. Nilforoushan D, Shirazi M, Dehpour AR. The role of opioid systems on orthodontic tooth movement in cholestatic rats. Angle Orthod 2002; 72:476-480.
6
7. Chao CF, Shih C, Wang TM, Lo TH. Effects of prostaglandin E2 on alveolar bone resorption during orthodontic tooth movement. Acta Anat (Basel) 1988; 132:304-309.
7
8. Kale S, Kocadereli I, Atilla P, Aşan E. Comparison of the effects of 1,25 dihydroxycholecalciferol and prostaglandin E2 on orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2004; 25:607-614.
8
9. Bartzela T, Turp JC, Motschall E, Maltha JC. Medication effects on the rate of orthodontic tooth movement: a systematic literature review. Am J Orthod Dentofacial Orthop 2009; 135:16-26.
9
10. Fredholm BB, Battig K, Holmen J, Nehlig A, Zvartau EE. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 1999; 51:83-133.
10
11. Kinoshita T, Kobayashi S, Ebara S, Yoshimura Y, Horiuchi H, Tsutsumimoto T, et al. Phosphodiesterase inhibitors, pentoxifylline and rolipram, increase bone mass mainly by promoting bone formation in normal mice. Bone 2000; 27:811-817.
11
12. Mediero A, Cronstein BN. Adenosine and bone metabolism. Trends Endocrinol Metab 2013; 24:290-300.
12
13. Bruton L, Chabner B, Knollman B. Goodman and Gilman's The Pharmacological Basis of Therapeutics. New York: McGrawhill; 2011.
13
14. Barcelos RP, Souza MA, Amaral GP, Stefanello ST, Bresciani G, Fighera MR, et al. Caffeine intake may modulate inflammation markers in trained rats. Nutrients 2014; 6:1678-1690.
14
15. Bezerra JP, da Silva LR, de Alvarenga Lemos VA, Duarte PM, Bastos MF. Administration of high doses of caffeine increases alveolar bone loss in ligature-induced periodontitis in rats. J Periodontol 2008; 79: 2356-2360.
15
16. Rapuri PB, Gallagher JC, Kinyamu HK, Ryschon KL. Caffeine intake increases the rate of bone loss in elderly women and interacts with vitamin D receptor genotypes. Am J Clin Nutr 2001; 74:694-700.
16
17. Tsuang YH, Sun JS, Chen LT, Sun SC, Chen SC. Direct effects of caffeine on osteoblastic cells metabolism: the possible causal effect of caffeine on the formation of osteoporosis. J Orthop Surg Res 2006; 1:7.
17
18. Sakamoto W, Nishihira J, Fujie K,Iizuka T, Handa H, Ozaki M, et al. Effect of coffee consumption on bone metabolism. Bone 2001; 28:332-336.
18
19. Duarte PM, Marques MR, Bezerra JP, Bastos MF. The effects of caffeine administration on the early stage of bone healing and bone density A histometric study in rats. Arch Oral Biol 2009; 54:717-722.
19
20. Nawrot P, Jordan S, Eastwood J, Rotstein J, Hugenholtz A, Feeley M. Effects of caffeine on human health. Food Addit Contam 2003; 20:1-30.
20
21. Folwarczna J, Pytlik M, Zych M, Cegieła U, Kaczmarczyk-Sedlak I, Nowińska B, et al. Favorable effect of moderate dose caffeine on the skeletal system in ovariectomized rats. Mol Nutr Food Res 2013; 57:1772-1784.
21
22. Grabrucker AM1, Rowan M, Garner CC. Brain-Delivery of Zinc-Ions as Potential Treatment for Neurological Diseases: Mini Review. Drug Deliv Lett 2011; 1:13-23.
22
23. Shirazi M, Alimoradi H, Kheirandish Y, Etemad-Moghadam S, Alaeddini M, Meysamie A, et al. Pantoprazole, a proton pump inhibitor, increases orthodontic tooth movement in rats. Iran J Basic Med Sci 2014; 17:448-453.
23
24. Sekhavat AR, Mousavizadeh K, Pakshir HR, Aslani FS. Effect of misoprostol, a prostaglandin E1 analog, on orthodontic tooth movement in rats. Am J Orthod Dentofacial Orthop 2002; 122:542-547.
24
25. Jager A, Zhang D, Kawarizadeh A, Tolba R, Braumann B, Lossdörfer S, Götz W. Soluble cytokine receptor treatment in experimental orthodontic tooth movement in the rat. Eur J Orthod 2005; 27:1-11.
25
26. Horrigan LA, Kelly JP, Connor TJ. Caffeine suppresses TNF-alpha production via activation of the cyclic AMP/protein kinase A pathway. Int Immunopharmacol 2004; 4:1409-1417.
26
27. Bruynzeel I, Stoof TJ, Willemze R. Pentoxifylline and skin inflammation. Clin Exp Dermatol 1998; 23:168-172.
27
28. Yi J, Zhang L, Yan B, Yang L, Li Y, Zhao Z. Drinking coffee may help accelerate orthodontic tooth movement. Dent Hypotheses 2012; 3:72-75.
28
29. Peng S, Yong-chun H. Effect of caffeine on alveolar bone remodeling during orthodontic tooth movement in rats. J Tongji Univ 2011; 3:9-29.
29
30. Yi J, Yan B, Li M, Wang Y, Zheng W, Li Y, et al. Caffeine may enhance orthodontic tooth movement through increasing osteoclastogenesis induced by periodontal ligament cells under compression. Arch Oral Biol 2016; 64:51-60.
30
31. Su SJ, Chang KL, Su SH, Yeh YT, Shyu HW, Chen KM. Caffeine regulates osteogenic differentiation and mineralization of primary adipose-derived stem cells and a bone marrow stromal cell line. Int J Food Sci Nutr 2013; 64:429-436.
31
ORIGINAL_ARTICLE
Comparative proteome analysis of human esophageal cancer and adjacent normal tissues
Objective(s): Ranking as the sixth commonest cancer, esophageal squamous cell carcinoma (ESCC) represents one of the leading causes of cancer death worldwide. One of the main reasons for the low survival of patients with esophageal cancer is its late diagnosis. Materials and Methods: We used proteomics approach to analyze ESCC tissues with the aim of a better understanding of the malignant mechanism and searching candidate protein biomarkers for early diagnosis of esophageal cancer. The differential protein expression between cancerous and normal esophageal tissues was investigated by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE). Then proteins were identified by matrix-assisted laser desorption/ ionization tandem time-of-flight mass spectrometry (MALDI-TOF/TOF-MS) and MASCOT web based search engine. Results:We reported 4 differentially expressed proteins involved in the pathological process of esophageal cancer, such as annexinA1 (ANXA1), peroxiredoxin-2 (PRDX2), transgelin (TAGLN) andactin-aortic smooth muscle (ACTA2). Conclusion: In this report we have introduced new potential biomarker (ACTA2). Moreover, our data confirmed some already known markers for EC in our region.
https://ijbms.mums.ac.ir/article_8354_051cb90ae4d763bd04d61aa0a6d6ee93.pdf
2017-03-01
265
271
10.22038/ijbms.2017.8354
Annexin
Actin-aortic smooth muscle Esophageal cancer
Proteomics
Peroxiredoxin
Transgelin
Two-dimensional-electrophoresis (2D)
Rezvan
Yazdian–Robati
1
Department of Pharmaceutical Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Homa
Ahmadi
ahmadim901@mums.ac.ir
2
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Maryam
Matbou Riahi
riahim@mums.ac.ir
3
Department of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Parisa
Lari
4
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Amir
Aledavood
5
Cancer Research Center, Department of Radiation oncology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Marzieh
Rashedinia
rashediniam@gmail.com
6
Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Iran
AUTHOR
Khalil
Abnous
7
Pharmaceutical Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad
Ramezani
ramezanim@mums.ac.ir
8
Nanotechnology Research Center, Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad Iran
LEAD_AUTHOR
1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden ofcancer in 2008. Int J Cancer 2010; 127:2893-2917.
1
2. Qi YJ, Chao WX, Chiu JF. An overview of esophageal squamous cell carcinoma proteomics. J Proteomics 2012;8;75:3129-3137.
2
3. Rice TW, Rusch VW, Apperson-Hansen C, Allen MS, Chen LQ, Hunter JG, et al. World wide esophageal cancer collaboration. Dis Esophagus 2009; 22:1-8.
3
4. Cho HJ, Baek KE, Park SM, Kim IK, Choi YL, Cho HJ, et al. RhoGDI2 expression is associated with tumor growth and malignant progression of gastric cancer. Clin Cancer Res 2009; 15:2612-2619.
4
5. Hongsachart P, Huang-Liu R, Sinchaikul S, Pan FM, Phutrakul S, Chuang YM, et al. Glycoproteomic analysis of WGA-bound glycoprotein biomarkers in sera from patients with lungadenocarcinoma.Electrophoresis 2009; 30:1206-1220.
5
6. Schulz DM, Bollner C, Thomas G, Atkinson M, Esposito I, Hofler H, et al. Identification of differentially expressed proteins in triple-negative breast carcinomas using DIGE and mass spectrometry.J Proteome Res. 2009;8:3430-3438.
6
7. Mathivanan S, Lim JW, Tauro BJ, Ji H, Moritz RL, Simpson RJ. Proteomics analysis of A33immunoaffinity-purified exosomes released from the human colon tumor cell line LIM1215 reveals atissue-specific protein signature. Mol Cell Proteomics 2010;9:197-208.
7
8. Ono M, Matsubara J, Honda K, Sakuma T, Hashiguchi T, Nose H, et al. Prolyl 4-hydroxylation ofalpha-fibrinogen: a novel protein modification revealed by plasma proteomics. J Biol Chem 2009; 284:29041-29049.
8
9. Vellaichamy A, Sreekumar A, Strahler JR, Rajendiran T, Yu J, Varambally S, et al. Proteomic interrogation of androgen action in prostate cancer cells reveals roles of aminoacyl tRNA synthetases. PLoS One 2009; 18;4:e7075
9
10. Uemura N, Kondo T. Current advances in esophageal cancer proteomics. Biochim Biophys Acta 2014: 1854:687-695.
10
11. Moghanibashi M, Zare M, Jazii FR. Proteomics and Esophageal Cancer. esophageal cancer–cell and molecular biology, biomarkers, nutrition and treatment 2012:83-85.
11
12. Uemura N, Kondo T. Current advances in esophageal cancer proteomics. Biochimicaet BiophysicaActa (BBA)-Proteins and Proteomics 2014: 1854:687-695.
12
13. Moghanibashi M, Jazii FR, Soheili Z-S, Zare M, Karkhane A, Parivar K, et al. Proteomics of a newesophageal cancer cell line established from Persian patient. Gene 2012; 500:124-133.
13
14. Jazii FR, Najafi Z, Malekzadeh R, Conrads TP, Ziaee AA, Abnet C, et al. Identification of squamouscell carcinoma associated proteins by proteomics and loss of beta tropomyosin expression in esophagealcancer. World journal of gastroenterology: WJG. 2006; 12:7104-7012.
14
15. Mi H, Lazareva-Ulitsky B, Loo R, Kejariwal A, Vandergriff J, Rabkin S, et al. The PANTHERdatabase of protein families, subfamilies, functions and pathways. Nucleic Acids Res 2005; 33: 284-288.
15
16. Flower RJ, Rothwell NJ. Lipocortin-1: cellular mechanisms and clinical relevance. Trends Pharmacol Sci 1994;15:71-76.
16
17. Perretti M, Gavins FN. Annexin 1: an endogenous anti-inflammatory protein. News Physiol Sci 2003;18:60-64.
17
18. Mussunoor S, Murray GI. The role of annexins in tumour development and progression. J Pathol 2008; 216:131-140.
18
19. Gerke V, Moss SE. Annexins: from structure to function. Physiol Rev. 2002; 82:331-3371.
19
20. Bastian BC. Annexins in cancer and autoimmune diseases. Cell Mol Life Sci 1997; 53:554-556.
20
21. Paweletz CP, Ornstein DK, Roth MJ, Bichsel VE, Gillespie JW, Calvert VS, et al. Loss of annexin 1correlates with early onset of tumorigenesis in esophageal and prostate carcinoma. Cancer Res.2000;60:6293-6297.
21
22. Hippo Y, Yashiro M, Ishii M, Taniguchi H, Tsutsumi S, Hirakawa K, et al. Differential geneexpression profiles of scirrhous gastric cancer cells with high metastatic potential to peritoneum orlymph nodes. Cancer Res 2001; 61:8890-8895.
22
23. Garcia Pedrero JM, Fernandez MP, Morgan RO, Herrero Zapatero A, Gonzalez MV, Suarez Nieto C, et al. Annexin A1 down-regulation in head and neck cancer is associated with epithelial differentiationstatus. Am J Pathol 2004; 164:73-79.
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24. Schwartz-Albiez R, Koretz K, Moller P, Wirl G. Differential expression of annexins I and II innormal and malignant human mammary epithelial cells. Differentiation 1993; 52:229-237.
24
25. Shen D, Chang HR, Chen Z, He J, Lonsberry V, Elshimali Y, et al. Loss of annexin A1 expression inhuman breast cancer detected by multiple high-throughput analyses. Biochem Biophys Res Commun 2005; 326:218-227.
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26. Alldridge LC, Harris HJ, Plevin R, Hannon R, Bryant CE. The annexin protein lipocortin 1 regulatesthe MAPK/ERK pathway. J Biol Chem 1999; 274:37620-37628.
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27. Alldridge LC, Bryant CE. Annexin 1 regulates cell proliferation by disruption of cell morphologyand inhibition of cyclin D1 expression through sustained activation of the ERK1/2 MAPK signal. Exp CellRes 2003; 290:93-107.
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28. Shen D, Nooraie F, Elshimali Y, Lonsberry V, He J, Bose S, et al. Decreased expression of annexinA1 is correlated with breast cancer development and progression as determined by a tissue microarrayanalysis. Hum Pathol. 2006; 37:1583-1591.
28
29. Xia SH, Hu LP, Hu H, Ying WT, Xu X, Cai Y, et al. Three isoforms of annexin I are preferentiallyexpressed in normal esophageal epithelia but down-regulated in esophageal squamous cell carcinomas.Oncogene 2002; 21:6641-6648.
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53. Li Y, Qin X, Cui J, Dai Z, Kang X, Yue H, et al. Proteome analysis of aflatoxin B1-inducedhepatocarcinogenesis in tree shrew (Tupaiabelangerichinensis) and functional identifi-cation ofcandidate protein peroxiredoxin II. Proteomics 2008; 8:1490-1501.
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56
ORIGINAL_ARTICLE
Scutellarin may alleviate cognitive deficits in a mouse model of hypoxia by promoting proliferation and neuronal differentiation of neural stem cells
Objective(s): Scutellarin, a flavonoid extracted from the medicinal herb Erigeron breviscapus Hand-Mazz, protects neurons from damage and inhibits glial activation. Here we examined whether scutellarin may also protect neurons from hypoxia-induced damage. Materials and Methods: Mice were exposed to hypoxia for 7 days and then administered scutellarin (50 mg/kg/d) or vehicle for 30 days Cognitive impairment in the two groups was assessed using the Morris water maze test, cell proliferation in the hippocampus was compared using 5-bromo-2-deoxyuridine (BrdU) immunohistochemistry, and hippocampal levels of nestin and neuronal class III β-tubulin (Tuj-1) were measured using Western blotting. These results were validated in vitro by treating cultured neural stem cells (NSCs) with scutellarin (30 μM). Results: Treating mice with scutellarin shortened escape times and increased the number of platform crossings, it increased the number of BrdU-positive proliferating cells in the hippocampus, and it up-regulated expression of nestin and Tuj-1. Treating NSC cultures with scutellarin increased the number of proliferating cells and the proportion of cells differentiating into neurons instead of astrocytes. The increase in NSC proliferation was associated with phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, while neuronal differentiation was associated with altered expression of differentiation-related genes. Conclusion: Scutellarin may alleviate cognitive impairment in a mouse model of hypoxia by promo-ting proliferation and neuronal differentiation of NSCs.
https://ijbms.mums.ac.ir/article_8355_f857416fa504aeaffc78daea53a1bbef.pdf
2017-03-01
272
279
10.22038/ijbms.2017.8355
Cognitive deficits
Differentiation
Hypoxia
Neural stem cells
Proliferation
Scutellarin
Wei-Wei
Wang
1
Department of Cardiology,China
AUTHOR
Jian-Hong
Han
hongjh8@126.com
2
The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, PR China
AUTHOR
Lin
Wang
kecheng1216@163.com
3
The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, PR China
AUTHOR
Tian-Hao
Bao
doctor@whu.edu.cn
4
The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, PR China
LEAD_AUTHOR
1. Sola S, Aranha MM, Rodrigues CM. Driving apoptosis-relevant proteins toward neural differentiation. Mol Neurobiol 2012; 46:316-331.
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2. Suh H, Deng W, Gage FH. Signaling in adult neurogenesis. Annu Rev Cell Dev Biol 2009; 25:253-275.
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3. Acharya MM, Martirosian V, Chmielewski NN, Hanna N, Tran KK, Liao AC, et al. Stem cell transplantation reverses chemotherapy-induced cognitive dysfunction. Cancer Res 2015; 75:676-686.
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4. Marei HE, Farag A, Althani A, Afifi N, Abd-Elmaksoud A, Lashen S, et al. Human olfactory bulb neural stem cells expressing hNGF restore cognitive deficit in Alzheimer's disease rat model. J Cell Physiol 2015; 230:116-130.
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5. Hassanzadeh K, Nikzaban M, Moloudi MR, Izadpanah E. Effect of selegiline on neural stem cells differentiation: a possible role for neurotrophic factors. Iran J Basic Med Sci 2015; 18:549-554.
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6. Yiming L, Wei H, Aihua L, Fandian Z. Neuroprotective effects of breviscapine against apoptosis induced by transient focal cerebral ischaemia in rats. J Pharm Pharmacol 2008; 60:349-355.
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7. Wang S, Wang H, Guo H, Kang L, Gao X, Hu L. Neuroprotection of Scutellarin is mediated by inhibition of microglial inflammatory activation. Neuroscience 2011; 185:150-160.
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8. Guo LL, Guan ZZ, Huang Y, Wang YL, Shi JS. The neurotoxicity of beta-amyloid peptide toward rat brain is associated with enhanced oxidative stress, inflammation and apoptosis, all of which can be attenuated by scutellarin. Exp Toxicol Pathol 2013; 65:579-584.
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9. Hong H, Liu GQ. Scutellarin protects PC12 cells from oxidative stress-induced apoptosis. J Asian Nat Prod Res 2007; 9:135-143.
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10. Xu W, Zha RP, Wang WY, Wang YP. Effects of scutellarin on PKCgamma in PC12 cell injury induced by oxygen and glucose deprivation. Acta Pharmacol Sin 2007; 28:1573-1579.
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11. Guo H, Hu LM, Wang SX, Wang YL, Shi F, Li H, et al. Neuroprotective effects of scutellarin against hypoxic-ischemic-induced cerebral injury via augmentation of antioxidant defense capacity. Chin J Physiol 2011; 54:399-405.
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12. Liu M, Li H, Luo G, Liu Q, Wang Y. Pharmacokinetics and biodistribution of surface modification polymeric nanoparticles. Arch Pharm Res 2008; 31:547-554.
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13. Wang WW, Lu L, Bao TH, Zhang HM, Yuan J, Miao W, et al. Scutellarin Alleviates Behavioral Deficits in a Mouse Model of Multiple Sclerosis, Possibly Through Protecting Neural Stem Cells. J Mol Neurosci 2016; 58:210-220.
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14. Chai L, Guo H, Li H, Wang S, Wang YL, Shi F, et al. Scutellarin and caffeic acid ester fraction, active components of Dengzhanxixin injection, upregulate neurotrophins synthesis and release in hypoxia/-reoxygenation rat astrocytes. JEthnopharmacol 2013; 150:100-107.
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15. Liu D, Wang Z, Zhan J, Zhang Q, Wang J, Zhang Q, et al. Hydrogen sulfide promotes proliferation and neuronal differentiation of neural stem cells and protects hypoxia-induced decrease in hippocampal neurogenesis. Pharmacol Biochem Behav 2014; 116:55-63.
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16. Lin LL, Liu AJ, Liu JG, Yu XH, Qin LP, Su DF. Protective effects of scutellarin and breviscapine on brain and heart ischemia in rats. J Cardiovasc Pharmacol 2007; 50:327-332.
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17. Jin G, Bai D, Yin S, Yang Z, Zou D, Zhang Z, et al. Silibinin rescues learning and memory deficits by attenuating microglia activation and preventing neuroinflammatory reactions in SAMP8 mice. Neurosci Lett 2016; 629:256-261.
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18. Zhu YH, Zhang CW, Lu L, Demidov ON, Sun L, Yang L, et al. Wip1 regulates the generation of new neural cells in the adult olfactory bulb through p53-dependent cell cycle control. Stem Cells 2009; 27:1433-1442.
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19. Wu XS, Bao TH, Ke Y, Sun DY, Shi ZT, Tang HR, et al. Hint1 suppresses migration and invasion of hepatocellular carcinoma cells in vitro by modulating girdin activity. Tumour Biol 2016 ; 37:14711-14719.
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20. Schwindt TT, Motta FL, Gabriela FB, Cristina GM, Guimaraes AO, Calcagnotto ME, et al. Effects of FGF-2 and EGF removal on the differentiation of mouse neural precursor cells. An Acad Bras Cienc 2009; 81:443-452.
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21. Kim YH, Chung JI, Woo HG, Jung YS, Lee SH, Moon CH, et al. Differential regulation of proliferation and differentiation in neural precursor cells by the Jak pathway. Stem Cells 2010; 28:1816-1828.
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24. Wang PS, Wang J, Zheng Y, Pallen CJ. Loss of protein-tyrosine phosphatase alpha (PTPalpha) increases proliferation and delays maturation of oligodendrocyte progenitor cells. J Biol Chem 2012; 287:12529-12540.
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25.Veazey KJ, Carnahan MN, Muller D, Miranda RC, Golding MC. Alcohol-induced epigenetic alterations to developmentally crucial genes regulating neural stemness and differentiation. Alcohol Clin Exp Res 2013; 37:1111-1122.
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26. Kennea NL, Mehmet H. Neural stem cells. J Pathol 2002; 197:536-550.
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27. Piao CS, Li B, Zhang LJ, Zhao LR. Stem cell factor and granulocyte colony-stimulating factor promote neuronal lineage commitment of neural stem cells. Differentiation 2012; 83:17-25.
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28. Chu T, Zhou H, Wang T, Lu L, Li F, Liu B, et al. In vitro characteristics of valproic acid and all-trans-retinoic acid and their combined use in promoting neuronal differentiation while suppressing astrocytic differentiation in neural stem cells. Brain Res 2015;1596:31-47.
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29. Eendebak RJ, Lucassen PJ, Fitzsimons CP. Nuclear receptors and microRNAs: Who regulates the regulators in neural stem cells. FEBS Lett 2011; 585:717-722.
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31. Muthuraju S, Maiti P, Solanki P, Sharma AK, Amitabh, Singh SB, et al. Acetylcholinesterase inhibitors enhance cognitive functions in rats following hypobaric hypoxia. Behav Brain Res 2009; 203:1-14.
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35. Wang Z, Liu DX, Wang FW, Zhang Q, Du ZX, Zhan JM, et al. L-Cysteine promotes the proliferation and differentiation of neural stem cells via the CBS/H(2)S pathway. Neuroscience 2013; 237:106-117.
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36. Kageyama R, Ohtsuka T, Hatakeyama J, Ohsawa R. Roles of bHLH genes in neural stem cell differentiation. Exp Cell Res 2005; 306:343-348.
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37. Kageyama R, Ohtsuka T, Kobayashi T. Roles of Hes genes in neural development. Dev Growth Differ 2008;1:S97-103.
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38. Katakura M, Hashimoto M, Shahdat HM, Gamoh S, Okui T, Matsuzaki K, et al. Docosahexaenoic acid promotes neuronal differentiation by regulating basic helix-loop-helix transcription factors and cell cycle in neural stem cells. Neuroscience 2009; 160:651-660.
38
ORIGINAL_ARTICLE
Cadmium chloride treatment of rats significantly impairs membrane integrity of mesenchymal stem cells via electrolyte imbalance and lipid peroxidation, a possible explanation of Cd related osteoporosis
Objective(s): Bone marrow mesenchymal stem cells (MSCs) play an important role in bone health. Cadmium causes osteoporosis, but the exact mechanisms of its effect on MSCs are not known. Materials and Methods: Rats were treated with cadmium chloride (40 mg/l) in drinking water for six weeks, and then the biochemical and morphological studies on MSCs were carried out as a cellular backup for osteoblasts. Viability and proliferation properties of the cells were evaluated using MTT assay, trypan blue, population doubling number, and colony forming assay. Morphology of the cells and biochemical parameters including activity of metabolic (ALP, AST, and ALT) and antioxidant enzymes (SOD, CAT, and POX) as well as the MDA level (as an indication of lipid peroxidation) were investigated. In addition, intracellular calcium, potassium, and sodium content were estimated. Data was analyzed statistically and P Results: The results showed a significant reduction in viability and proliferation ability of extracted cells when compared to the controls. In addition, it was revealed that the cadmium treatment of rats caused a significant reduction in nuclear diameter and cytoplasm area. Also, there was significant increase in (ALT) and (AST) activity and intracellular calcium and potassium content but no change was observed with sodium content and ALP activity. The results showed [a] significant reduction in the antioxidant enzyme activity and increases in the MDA level. Conclusion: Based on the present study, reduction of viability and proliferation ability of MSCs might be a causative factor of osteoporosis in industrial areas.
https://ijbms.mums.ac.ir/article_8356_305d6cfabde54feaec28c36dcaf73c37.pdf
2017-03-01
280
287
10.22038/ijbms.2017.8356
Alanine transaminase
Aspartate transaminase
Lipid Peroxidation
MSCs
Proliferation
Viability
Mohammad Husein
Abnosi
m-abnosi@araku.ac.ir
1
Department of Biology, Faculty of Sciences, Arak University, Arak, Iran
LEAD_AUTHOR
Someyeh
Golami
2
Department of Biology, Faculty of Sciences, Arak University, Arak, Iran
AUTHOR
1. ATSDR. Toxicological Profile for Cadmium. Agency for Toxic Substances and Disease Registry, US Department of Health and Human Services. 1999.Available at: URL: http://www.atsdr.cdc.gov/toxprofiles/tp5.html.
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2
3. Nair AR, DeGheselle O, Smeets K, Van Kerkhove E, Cuypers A. Cadmium-induced pathologies: where is the oxidative balance lost (or Not)? Int J Mol Sci 2013; 14:6116-6143.
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8. Satarug S, Moore MR. Adverse health effects of chronic exposure to low-level cadmium in foodstuffs and cigarette smoke. Environ Health Perspect 2004; 112:1099–1103.
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14. Giaginis C, Gatzidou E, Theocharis S. DNA repair systems as targets of cadmium toxicity. Toxicol Appl Pharmacol 2006; 213:282–290.
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15. Ogawa T, Kobayashi E, Okubo Y, Suwazono Y, Kido T, Nogawa K. Relationship among prevalence of patients with Itai-itai disease, prevalence of abnormal urinary findings, and cadmium concentrations in rice of individual hamlets in the Jinzu River basin, Toyama prefecture of Japan. Int J Environ Health Res 2004; 14:243–252.
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17. Åkesson A, Bjellerup P, Lundh T, Lidfeldt J, Nerbrand C, Samsioe G, et al. Cadmium-induced effects on bone in a population-based study of women. Environ Health Perspect 2006; 114:830–834.
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18. Kazantzis G. Cadmium, osteoporosis and calcium metabolism. Biometals 2004; 17:493-498.
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19. Engström A, Skerving S, Lidfeldt J, Burgaz A, Lundh T, Samsioe G, et al. Cadmium-induced bone effect is not mediated via low serum 1,25-dihydroxy vitamin D. Environ Res 2009; 109:188–192.
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20. Wallin M, Sallsten G, Fabricius-Lagging E, Öhrn C, Lundh T, Barregard L. Kidney cadmium levels and associations with urinary calcium and bone mineral density: a cross-sectional study in Sweden. Environ Health 2013; 12:22.
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21. Alghasham A, Salem TA, Meki AR. Effect of cadmium-polluted water on plasma levels of tumor necrosis factor-alpha, interleukin-6 and oxidative status biomarkers in rats: protective effect of curcumin. Food Chem Toxicol 2013; 59:160-164
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22. El-Boshy ME, Risha EF, Abdelhamid FM, Mubarak MS, Hadda TB. Protective effects of selenium against cadmium induced hematological disturbances, immunosuppressive, oxidative stress and hepatorenal damage in rats. J Trace Elem Med Biol 2015; 29:104-110.
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23. Baghaban Eslaminejad M, Salami F, Soleymani Mehranjani M, Abnoosi MH, Eftekhari-Yazdi P. Bromoindirubin-3-oxime treatment enhances the in vitro proliferation and viability of rat marrow-derived mesenchymal stem cells. Physiol Pharmacol 2009; 13:57–67.
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24. Greco SJ, Zhou C, Ye JH, Rameshwar P. A method to generate human mesenchymal stem cell-derived neurons which express and are excited by multiple neurotransmitters. Biol Proced Online 2008; 10: 90-101.
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44
ORIGINAL_ARTICLE
Mutation analysis of connexin 50 gene among Iranian families with autosomal dominant cataracts
Objective(s): Childhood cataract is a genetically heterogeneous eye disorder that results in visual impairment. The aim of this study was to identify the genetic mutations of connexin 50 gene among Iranian families suffered from autosomal dominant congenital cataracts (ADCC). Materials and Methods: Families, having at least two members with bilateral familial congenital cataract, were selected for the study. Probands were evaluated by detailed ophthalmologist’s examination, and the pedigree analysis was performed. PCR amplifications were performed corresponding to coding region and intron-exon boundaries of GJA8, a candidate gene responsible for ADCC. PCR products were subjected to bidirectional sequencing, and the co-segregation of identified mutations was examined and finally, the impact of identified mutations on biological functions of GJA8 was predicted by in silico examination. Results: Three different genetic alterations, including c.130G>A (p.V44M), c.301G>T (p.R101L) and c.134G>T (p.W45L) in GJA8 gene were detected among three probands. Two identified mutations, W45L and V44M have been already reported, while the R101L is a novel mutation and its co-segregation was examined. This mutation was exclusively detected in the ADCC and could not be found among the healthy control group. The result of bioinformatic studies of R101L mutation predicted that this amino acid substitution within GJA8 could be a disease-afflicting mutation due to its potential effect on the protein structure and biological function. Conclusion: Our results suggest that mutations of lens connexin genes such as GJA8 gene could be one of the major mechanisms of cataract development, at least in a significant proportion of Iranian patients with ADCC.
https://ijbms.mums.ac.ir/article_8358_b07ad559443877d8ee1da6ef6617064c.pdf
2017-03-01
288
293
10.22038/ijbms.2017.8358
Cataract
Congenital
Connexine 50 gene
GJA8
Mutation
Masoumeh
Mohebi
mmohebi14@gmail.com
1
Farabi Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Saeed
Chenari
schenari@gmail.com
2
Farabi Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Abolfazl
Akbari
akbari@yahoo.com
3
Colorectal Research Center, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Fariba
Ghassemi
4
Farabi Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mehran
Zarei-Ghanavati
5
Farabi Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ghasem
Fakhraie
fakhraiegh@yahoo.com
6
Farabi Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Nahid
Babaie
7
Department of Molecular Biology and Genetics, Islamic Azad University, Bushehr Branch, Bushehr, Iran
AUTHOR
Mansour
Heidari
mheidari@sina.tums.ac.ir
8
Department of Molecular Biology and Genetics, Islamic Azad University, Bushehr Branch, Bushehr, Iran
LEAD_AUTHOR
1.Yi J, Yun J, Li ZK, Xu CT, Pan BR. Epidemiology and molecular genetics of congenital cataracts. Int J Ophthalmol, 2011; 4:422-432.
1
2.Mohebi M, Akbari A, Babaei N, Sadeghi A, Heidari M. Identification of a De Novo 3bp Deletion in CRYBA1/A3 Gene in Autosomal Dominant Congenital Cataract. Acta Med Iran 2016;54(12):778-783.
2
3.Rong X, Ji Y, Fang Y, Jiang Y, Lu Y. Long-Term Visual Outcomes of Secondary Intraocular Lens Implantation in Children with Congenital Cataracts. PLoS One 2015; 10:e0134864.
3
4.Sukhija J, Kaur S, Ram J. Outcome of a new acrylic intraocular lens implantation in pediatric cataract. J Pediatr Ophthalmol Strabismus 2015; 52:371-376.
4
5.Umar MM, Abubakar A, Achi I, Alhassan MB, Hassan A. Pediatric cataract surgery in National Eye Centre Kaduna, Nigeria: outcome and challenges. Middle East Afr J Ophthalmol 2015; 22:92-96.
5
6.Wang M, Xiao W. Congenital cataract: progress in surgical treatment and postoperative recovery of visual function. Eye Sci 2015; 30:38-47.
6
7.Hejtmancik JF, Smaoui N. Molecular genetics of cataract. Dev Ophthalmol 2003; 37:67-82.
7
8.Huang B, He W. Molecular characteristics of inherited congenital cataracts. Eur J Med Genet 2010; 53:347-57.
8
9.Deng H, Yuan L. Molecular genetics of congenital nuclear cataract. Eur J Med Genet 2014; 57:113-122.
9
10.Garnai SJ, Huyghe JR, Reed DM, Scott KM, Liebmann JM, Boehnke M, et al. Congenital cataracts: de novo gene conversion event in CRYBB2. Mol Vis 2014; 20:1579-1593.
10
11.He W, Li S. Congenital cataracts: gene mapping. Hum Genet 2000; 106:1-13.
11
12.Reddy MA, Francis PJ, Berry V, Bhattacharya SS, Moore AT. Molecular genetic basis of inherited cataract and associated phenotypes. Surv Ophthalmol 2004; 49:300-315.
12
13.Mobini G, Ghahremani M, Amanpour S, Dehpour A, Akbari A, Hoseiniharouni S, et al. Transforming growth factor beta-induced factor 2-linked X (TGIF2LX) regulates two morphogenesis genes, Nir1 and Nir2 in human colorectal. Acta Med Iran 2016; 54:302-307.
13
14.Akbari A, Ghahremani MH, Mobini GR, Abastabar M, Akhtari J, Bolhassani M, et al. Down-regulation of miR-135b in colon adenocarcinoma induced by a TGF-β receptor I kinase inhibitor (SD-208). Iran J Basic Med Sci 2015; 18:856-861.
14
15.Yazdi MK, Akbari A, Soltan Dallal MM. Multiplex polymerase chain reaction (PCR) assay for simultaneous detection of shiga-like toxin (stx1 and stx2), intimin (eae) and invasive plasmid antigen H (ipaH) genes in diarrheagenic Escherichia coli. Afr J Biotechnol 2011; 109:1522-1526.
15
16.Akbari A, Mobini GR, Maghsoudi R, Akhtari J, Faghihloo E, Farahnejad Z. Modulation of transforming growth factor-β signaling transducers in colon adenocarcinoma cells induced by staphylococcal enterotoxin B. Mol Med Rep 2016; 13:909-991.
16
17.Akbari A, Farahnejad Z, Akhtari J, Abastabar M, Mobini GR, Mehbod AS. Staphylococcus aureus Enterotoxin B Down-Regulates the Expression of Transforming Growth Factor-Beta (TGF-β) Signaling Transducers in Human Glioblastoma. Jundishapur J Microbiol 2016; 9:e27297.
17
18.Akbari A, Amanpour S, Muhammadnejad S, Ghahremani MH, Gaffari SH, Dehpour AR, et al. Evaluation of antitumor activity of a TGF-beta receptor I inhibitor (SD-208) on human colon adenocarcinoma. Daru J Pharm Sci. 2014;22:47–54.
18
19.Beyer EC, Berthoud VM. Connexin hemichannels in the lens. Front Physiol 2014; 5:20.
19
20.Chen C, Sun Q, Gu M, Liu K, Sun Y, Xu X. A novel Cx50 (GJA8) p.H277Y mutation associated with autosomal dominant congenital cataract identified with targeted next-generation sequencing. Graefes Arch Clin Exp Ophthalmol 2015; 253:915-924.
20
21.Jiang JX. Gap junctions or hemichannel-dependent and independent roles of connexins in cataractogenesis
21
and lens development. Curr Mol Med 2010; 10:851-863.
22
22.Li J, Wang Q, Fu Q, Zhu Y, Zhai Y, Yu Y, Zhang K, Yao K. A novel connexin 50 gene (gap junction protein, alpha 8) mutation associated with congenital nuclear and zonular pulverulent cataract. Mol Vis 2013; 19:767-774.
23
23.Minogue PJ, Tong JJ, Arora A, Russell-Eggitt I, Hunt DM, Moore AT, et al. A mutant connexin50 with enhanced hemichannel function leads to cell death. Invest Ophthalmol Vis Sci 2009; 50:5837-5845.
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24.Pfenniger A, Wohlwend A, Kwak BR. Mutations in connexin genes and disease. Eur J Clin Invest 2011; 41:103-116.
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25.Rubinos C, Villone K, Mhaske PV, White TW, Srinivas M. Functional effects of Cx50 mutations associated with congenital cataracts. Am J Physiol Cell Physiol 2014; 306:C212-220.
26
26.Zhu Y, Yu H, Wang W, Gong X, Yao K. Correction: A Novel GJA8 Mutation (p.V44A) Causing Autosomal Dominant Congenital Cataract. PLoS One 2015; 10:e0125949.
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27.Zhu Y, Yu H, Wang W, Gong X, Yao K. A novel GJA8 mutation (p.V44A) causing autosomal dominant congenital cataract. PLoS One 2014; 9:e115406.
28
28.Wang L, Luo Y, Wen W, Zhang S, Lu Y. Another evidence for a D47N mutation in GJA8 associated with autosomal dominant congenital cataract. Mol Vis 2011; 17:2380-2385.
29
29.Mackay DS, Bennett TM, Culican SM, Shiels A. Exome sequencing identifies novel and recurrent mutations in GJA8 and CRYGD associated with
30
inherited cataract. Hum Genomics 2014; 8:19.
31
30.Ren Q, Riquelme MA, Xu J, Yan X, Nicholson BJ, Gu S, et al. Cataract-causing mutation of human connexin 46 impairs gap junction, but increases hemichannel function and cell death. PLoS One 2013; 8:e74732.
32
31.Sarkar D, Ray K, Sengupta M. Structure-function correlation analysis of connexin50 missense mutations causing congenital cataract: electrostatic potential alteration could determine intracellular trafficking fate of mutants. Biomed Res Int 2014; 2014:673895.
33
ORIGINAL_ARTICLE
Detection of Th17/Treg cells and related factors in gingival tissues and peripheral blood of rats with experimental periodontitis
Objective(s): This study aimed to investigate the role and the possible mechanisms involved in the immunoregulation of experimental periodontitis by Th17/Treg. Materials and Methods: Experimental periodontitis was established by silk thread ligation with Porphyromonasgingivalis daubing in the bilateral maxillary second molar of Male Sprague-Dawley (SD) rats. Alveolar bones were scanned by Micro-CT. Histological examination was stained with H&E. The proportions of Th17 and Treg cells in peripheral blood were detected by flow cytometry. RT-PCR was used to measure the expression of RORγt, Foxp3 mRNA in the gingival tissues. The concentrations of IL-17, IL-10, and TGF-β in peripheral blood and gingival crevicular fluid were measured by ELISA. Results: Experimental rats showed profound bone resorption and inflammatory cell infiltration. The percentages of Th17 significantly increased in the peripheral blood, which was consistent with gingival tissues study that Th17 cells related transcription factor RORγt mRNA and IL-17 increased in the course of periodontitis. The percentages of CD25+Foxp3+ Treg significantly increased in the peripheral blood, which was consistent with gingival tissues study that Treg cells related transcription factor Foxp3 mRNA and cytokines IL-10 and TGF-β increased in the course of periodontitis. The ratio of Th17/Treg cells was significantly increased in the peripheral circulation, however, the Th17/Treg balance is in wave motion in inflamed gingival tissues in the different stages of periodontitis. Conclusion: Th17/Treg balance may be associated with the progression of periodontitis and pathological tissue destruction. Moreover, local inflammation would result in the up-regulation ratio of Th17/Treg in peripheral blood, which may influence some periodontally involved systemic diseases.
https://ijbms.mums.ac.ir/article_8359_bd8a5dd5f6f194deb032e38afaf0578e.pdf
2017-03-01
294
300
10.22038/ijbms.2017.8359
Bone resorption
Cytokine
Experimental periodontitis
Th17
Treg
Li
Gao
li__gao@sina.com
1
Department of Periodontology, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat -sen University, Guangzhou 510055,China
AUTHOR
Yajing
Zhao
2
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
AUTHOR
Panpan
Wang
3
Department of Periodontology, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat -sen University, Guangzhou 510055,China
AUTHOR
Liping
Zhang
4
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
AUTHOR
Chi
Zhang
zhangchi9966@163.com
5
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
AUTHOR
Qianying
Chen
6
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
AUTHOR
Chuanjiang
Zhao
zhaochj@mail.sysu.edu.cn
7
Department of Periodontology, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat -sen University, Guangzhou 510055,China
LEAD_AUTHOR
1. Lavu V, Venkatesan V, Rao SR.The epigenetic paradigm in periodontitis pathogenesis. J Indian Soc Periodontol 2015;19:142-149.
1
2. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nat Rev Immunol 2014;15:30-44.
2
3. Llambés F, Arias-Herrera S, Caffesse R. Relationship between diabetes and periodontal infection.World J Diabetes 2015;6:927-935.
3
4. Kholy KE, Genco RJ, Van Dyke TE. Oral infections and cardiovascular disease. Trends Endocrinol Metab 2015; 26:315-321.
4
5. Hussain M, Stover CM, Dupont A. P.gingivalis in Periodontal Disease and Atherosclerosis-Scenes of Action for Antimicrobial Peptides and Complement. Front Immunol 2015; 6: 45.
5
6. Hernández M, Dutzan N, García-Sesnich J, Abusleme L, Dezerega A, Silva N, et al. Host-pathogen interactions in progressive chronic periodontitis. J Dent Res 2011; 90:1164-1170.
6
7. Teng YT. The role of acquired immunity and periodontal disease progression. Crit Rev Oral Biol Med 2003;14:237-252.
7
8. Gemmell E, Yamazaki K, Seymour GJ. The role of T cells in periodontal disease: homeostasis and autoimmunity. Periodontol 2007;43:14-40.
8
9. Graves D. Cytokines that promote periodontal tissue destruction. J Periodontol 2008; 79:1585-1591.
9
10. Peters A, Lee Y, Kuchroo VK. The many faces of Th17 cells. Curr Opin Immunol 2011; 23:702-706.
10
11. Isailovic N, Daigo K, Mantovani A, Selmi C. Interleukin-17 and innate immunity in infections and chronic inflammation. J Autoimmun 2015; 60:1-11.
11
12. Miossec P, Kolls JK. Targeting IL-17 and TH17 cells in chronic inflammation. Nat Rev Drug Discov 2012; 11:763-776.
12
13. Hienz SA, Paliwal S, Ivanovski S. Mechanisms of Bone Resorption in Periodontitis. J Immunol Res 2015; 2015:615486.
13
14. Du Y, Chen X, Huang ZM, Ye XH, Niu Q. Increased frequency of Foxp3+ regulatory T cells in mice with hepatocellular carcinoma. Asian Pac J Cancer Prev 2013;13:3815-3819.
14
15. Haque M, Fino K, Lei F, Xiong X, Song J. Utilizing regulatory T cells against rheumatoid arthritis. Front Oncol 2014; 4:209.
15
16. Sakaguchi S. Naturally arising CD4+ regulatory T-cells for immunologic self-tolerance and negative control of immune responses. Annu Rev Immunol 2004; 22:531-562.
16
17. Garlet GP, Cardoso CR, Mariano FS, Claudino M, de Assis GF, Campanelli AP, et al. Regulatory T cells attenuate experimental periodontitis progression in mice. J Clin Periodontol 2010; 37:591-600.
17
18. Lee SY, Lee SH, Yang EJ, Kim EK, Kim JK, Shin DY, Cho ML. Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance. PLoS One 2015;10: e0135858.
18
19. Wei Y, Luo QL, Sun J, Chen MX, Liu F, Dong JC. Bu-Shen-Yi-Qi formulae suppress chronic airway inflammation and regulate Th17/Treg imbalance in the murine ovalbumin asthma model. J Ethnopharmacol 2015;164:368-377.
19
20. Duan MC, Zhong XN, Liu GN, Wei JR. The Treg/Th17 paradigm in lung cancer. J Immunol Res 2014; 2014:730380.
20
21. Li XS, Li S, Kellermann G. An integrated liquid chromatography-tandem mass spectrometry approach for the ultra-sensitive determination of catecholamines in human peripheral blood mononuclear cells to assess neural-immune communication.J Chromatogr A 2016;1449:54-61.
21
22. Bleda S,de Haro J,Varela C,Ferruelo A,Acin F. Elevated levels of triglycerides and vldl-cholesterol provoke activation of nlrp1 inflammasome in endothelial cells. Int J Cardiol 2016;220:52-55.
22
23. Imai K, Victoriano AF, Ochiai K, Okamoto T. Microbial interaction of periodontopathic bacterium Porphyromonas gingivalis and HIV-possible causal link of periodontal diseases to AIDS progression. Curr HIV Res 2012;10:238-244.
23
24. Norowski PA Jr, Bumgardner JD. Biomaterial and antibiotic strategies for peri-implantitis: a review. J Biomed Mater Res B Appl Biomater 2009; 88:530-543.
24
25. Wang L, Wang J, Jin Y, Gao H, Lin X. Oral administration of all-trans retinoic acid suppresses experimental periodontitis by modulating the Th17/Treg imbalance. J Periodontol 2014; 85:740-750.
25
26. Sato K, Suematsu A, Okamoto K, Yamaguchi A, Morishita Y, Kadono Y, et al. Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction. J Exp Med 2006; 203:2673-2682.
26
27. Vernal R, Dutzan N, Chaparro A, Puente J, Antonieta Valenzuela M, Gamonal J. Levels of interleukin-17 in gingival crevicular fluid and in supernatants of cellular cultures of gingival tissue from patients with chronic periodontitis. J Clin Periodontol 2005; 32:383-389.
27
28. Cardoso CR, Garlet GP, Crippa GE, Rosa AL, Júnior WM, Rossi MA, et al. Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease. Oral Microbiol Immunol 2009; 24:1-6.
28
29. Yu JJ, Ruddy MJ, Wong GC, Sfintescu C, Baker PJ, Smith JB, et al. An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor-dependent signals. Blood 2007;109:3794-3802.
29
30. Kobayashi R, Kono T, Bolerjack BA, Fukuyama Y, Gilbert RS, Fujihashi K, et al. Induction of IL-10-producing CD4+ T-cells in chronic periodontitis. J Dent Res 2011; 90:653-658.
30
31. Okui T, Aoki Y, Ito H, Honda T, Yamazaki K. The presence of IL-17+/FOXP3+ double-positive cells in periodontitis. J Dent Res 2012:91:574-579.
31
32. Jin Y, Wang LY , Liu DX, Lin XP. Tamibarotene modulates the local immune response in experimental periodontitis. Int Immunopharmacol 2014; 23:537-545.
32
ORIGINAL_ARTICLE
Emergence of signs of neural cells after exposure of bone marrow-derived mesenchymal stem cells to fetal brain extract
Objective(s): Nowadays much effort is being invested in order to diagnose the mechanisms involved in neural differentiation. By clarifying this, making desired neural cells in vitro and applying them into diverse neurological disorders suffered from neural cell malfunctions could be a feasible choice. Thus, the present study assessed the capability of fetal brain extract (FBE) to induce rat bone marrow-derived mesenchymal stem cells (BM-MSCs) toward neural cells. Materials and Methods: For this purpose, BM-MSCs were collected from rats and cultured and their mesenchymal properties were confirmed. After exposure of the BM-MSCs to fetal brain extract, the cells were evaluated and harvested at days 3 and 7 after treatment. Results: The BM-MSCs that were exposed to FBE changed their appearance dramatically from spindle shape to cells with dendrite-like processes. Those neural like processes were absent in the control group. In addition, a neural specific marker, vimentin, was expressed significantly in the treatment group but not in the negative control group. Conclusion: This study presented the FBE as a natural neural differentiation agent, which probably has required factors for making neurons. In addition, vimentin overexpression was observed in the treated group which confirms neuron-like cell differentiation of BM-MSCs after induction.
https://ijbms.mums.ac.ir/article_8360_2d381972261cd956c8eb09467b65ef76.pdf
2017-03-01
301
307
10.22038/ijbms.2017.8360
Bone marrow-mesenchymal- stem cells
Differentiation
Fetal brain extract
Neural cell
Vimentin
Iman
Razeghian Jahromi
razejahrom@gmail.com
1
Cardiovascular Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Davood
Mehrabani
davood_mehrabani@yahoo.com
2
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Ali
Mohammadi
msmohamadi@yahoo.com
3
Division of Biotechnology, Department of Pathobiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
AUTHOR
Mohammad Mahdi
Ghahramani Seno
4
Division of Biotechnology, Department of Pathobiology, School of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Mehdi
Dianatpour
mdianatpour@sums.ac.ir
5
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Shahrokh
Zare
zare.shahrokh@gmail.com
6
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Amin
Tamadon
tamadon@yahoo.com
7
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
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15. Rahmanifar F, Tamadon A, Mehrabani D, Zare S, Abasi S, Keshavarz S, et al. Histomorphometric evaluation of treatment of rat azoospermic seminiferous tubules by allotransplantation of bone marrow-derived mesenchymal stem cells. Iran J Basic Med Sci 2016; 19:653-661.
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16. Khajehahmadi Z, Mehrabani D, Ashraf MJ, Rahmanifar F, Tanideh N, Tamadon A, et al. Healing effect of conditioned media from bone marrow-derived stem cells in thioacetamide-induced liver fibrosis of rat. J Med Sci 2016; 15:1-9.
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17. Razeghian Jahromi I, Mehrabani D, Mohammadi A, Dianatpour M, Tamadon A, Zare S, et al. The effect of fetal rat brain extract on morphology of bone marrow-derived mesenchymal stem cells. Comp Clin Pathol 2016; 25:343-349.
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33. Wislet-Gendebien S, Leprince P, Moonen G, Rogister B. Regulation of neural markers nestin and GFAP expression by cultivated bone marrow stromal cells. J Cell Sci 2003; 116:3295-3302.
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34. Munoz-Sanjuan I, Brivanlou AH. Neural induction, the default model and embryonic stem cells. Nat Rev Neurosci 2002; 3:271-280.
34
ORIGINAL_ARTICLE
Protective effects of tanshinone IIA sodium sulfonate on ischemia-reperfusion-induced myocardial injury in rats
Objective(s): This study investigated the protective effect of tanshinone IIA sodium sulfonate (TSS) on ischemia-reperfusion (I/R) induced cardiac injury, and the underlying mechanism of action. Materials and Methods:Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by 24 hours' reperfusion. Half an hour before the left coronary artery ligation, rats were pretreated with TSS in three different dosages (15, 30, 70 mg/kg, IP). Twenty-four hours later, cardiac function was measured and the ratio of infarct size to area at risk (AAR) was calculated. Western blotting examined the expression of the inflammatory mediator high-mobility group box1 (HMGB-1), anti-apoptotic protein Bcl-2, pro-apoptotic mediators such as Bax and Caspase-3, markers of autophagy such as ratio of LC3B/LC3A and Beclin-1 expression. Results: Our results showed that TSS dose-dependently improves cardiac function, accompanied with decrease of HMGB1 level, increase of LC3B/LC3A ratio and increase of Beclin-1 expression. TSS treatment down-regulates Bax and Caspase-3 expression, while up-regulating Bcl-2 levels. Conclusion: TSS ameliorates I/R induced myocardial injury and improves cardiac function via reducing inflammation and apoptosis, while enhancing autophagy.
https://ijbms.mums.ac.ir/article_8361_d49cca63ad0e992964747456edf2563c.pdf
2017-03-01
308
315
10.22038/ijbms.2017.8361
Apoptosis
Autophagy
Ischemia/reperfusion (I/R)
Tanshinone IIA sodium-sulfonate (TSS)
Yun
Pan
794291018@qq.com
1
Department of Emergency, The First Affiliated Hospital, Soochow University, 188 Shi-Zi Road, Suzhou 215006, PR China
AUTHOR
Jin-Xian
Qian
szicu@sina.com
2
Department of Emergency, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, P.R. China
AUTHOR
Shi-Qi
Lu
lushiqi2004@126.com
3
Department of Emergency, The First Affiliated Hospital, Soochow University, 188 Shi-Zi Road, Suzhou 215006, PR China
AUTHOR
Jing-Wei
Chen
szszyxh@163.com
4
Department of Internal Medicine, The Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Yang-Su Road, Suzhou 215003, P.R. China
AUTHOR
Xiao-Dong
Zhao
xiaodong@medmail.com.cn
5
Department of Internal Medicine, The Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Yang-Su Road, Suzhou 215003, P.R. China
AUTHOR
Yan
Jiang
yjiang@suda.edu.cn
6
Department of Physiology, Medical College of Soochow University, 199 Ren-Ai Road, Dushu Lake Campus, Suzhou Industrial Park, Suzhou 215123, P.R. China
AUTHOR
Lin-Hui
Wang
wanglinhui@suda.edu.cn
7
Department of Physiology, Medical College of Soochow University, 199 Ren-Ai Road, Dushu Lake Campus, Suzhou Industrial Park, Suzhou 215123, P.R. China
AUTHOR
Guo-Xing
Zhang
zhangguoxing@suda.edu.cn
8
Department of Physiology, Medical College of Soochow University, 199 Ren-Ai Road, Dushu Lake Campus, Suzhou Industrial Park, Suzhou 215123, P.R. China
LEAD_AUTHOR
1. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke statistics--2013 update: a report from the American Heart Association. Circulation. 2013;127(1):e6.
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6. Kwak W, Ha YS, Soni N, Lee W, Park S-I, Ahn H, et al. Apoptosis imaging studies in various animal models using radio-iodinated peptide. Apoptosis 2015; 20:110-121.
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8. Zhai C-l, Zhang M-q, Zhang Y, Xu H-x, Wang J-m, An G-p, et al. Glycyrrhizin protects rat heart against ischemia-reperfusion injury through blockade of HMGB1-dependent phospho-JNK/Bax pathway. Acta Pharmacol Sin 2012; 33:1477-1487.
8
9. Ding H-S, Yang J, Chen P, Yang J, Bo S-Q, Ding J-W, et al. The HMGB1-TLR4 axis contributes to myocardial ischemia/reperfusion injury via regulation of cardiomyocyte apoptosis. Gene. 2013; 527:389-393.
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10. Depre C, Vatner SF. Cardioprotection in stunned and hibernating myocardium. Heart Fail Rev 2007; 12:307-317.
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11. Ma X, Liu H, Foyil SR, Godar RJ, Weinheimer CJ, Diwan A. Autophagy is impaired in cardiac ischemia-reperfusion injury. Autophagy 2012; 8:1394-1396.
11
12. Ma X, Liu H, Foyil SR, Godar RJ, Weinheimer CJ, Hill JA, et al. Impaired autophagosome clearance contributes to cardiomyocyte death in ischemia/reperfusion injury. Circulation 2012; 125:3170-3181.
12
13. Chen C, Hu L-X, Dong T, Wang G-Q, Wang L-H, Zhou X-P, et al. Apoptosis and autophagy contribute to gender difference in cardiac ischemia–reperfusion induced injury in rats. Life Sci 2013; 93:265-270.
13
14. Przyklenk K, Undyala VV, Wider J, Sala-Mercado JA, Gottlieb RA, Mentzer RM, Jr. Acute induction of autophagy as a novel strategy for cardioprotection: getting to the heart of the matter. Autophagy 2011; 7:432-433.
14
15. Kai G, Xu H, Zhou C, Liao P, Xiao J, Luo X, et al. Metabolic engineering tanshinone biosynthetic pathway in Salvia miltiorrhiza hairy root cultures. Metab Eng 2011; 13:319-327.
15
16. Pan L-L, Liu X-H, Jia Y-L, Wu D, Xiong Q-H, Gong Q-H, et al. A novel compound derived from danshensu inhibits apoptosis via upregulation of heme oxygenase-1 expression in SH-SY5Y cells. Biochim Biophys Acta 2013; 1830:2861-2871.
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17. Wu G-b, Zhou E-x, Qing D-x. Tanshinone II (A ) elicited vasodilation in rat coronary arteriole: Roles of nitric oxide and potassium channels. Eur J Pharmacol 2009; 617:102-107.
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18. Yin Y, Guan Y, Duan J, Wei G, Zhu Y, Quan W, et al. Cardioprotective effect of Danshensu against myocardial ischemia/reperfusion injury and inhibits apoptosis of H9c2 cardiomyocytes via Akt and ERK1/2 phosphorylation. Eur J Pharmacol 2013; 699:219-226.
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19. Wei B, Li WW, Ji J, Hu QH, Ji H. The cardioprotective effect of sodium tanshinone IIA sulfonate and the optimizing of therapeutic time window in myocardial ischemia/reperfusion injury in rats. Atherosclerosis 2014; 235:318-327.
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20. Zhang G-X, Kimura S, Murao K, Obata K, Matsuyoshi H, Takaki M. Inhibition of cytochrome c release by 10-N-nonyl acridine orange, a cardiolipin-specific dye, during myocardial ischemia-reperfusion in the rat. Am J Physiol Heart Circ Physiol 2010; 298:H433-H439.
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21. Yang R, Liu A, Ma X, Li L, Su D, Liu J. Sodium tanshinone IIA sulfonate protects cardiomyocytes against oxidative stress-mediated apoptosis through inhibiting JNK activation. J Cardiovasc Pharmacol 2008; 51:396-401.
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22. Scarfò L, Ghia P. Reprogramming cell death: BCL2 family inhibition in hematological malignancies. Immunol Lett 2013; 155:36-39.
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23. Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med 2007; 357:1121-35.
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24. Dominguez-Rodriguez A, Abreu-Gonzalez P, Reiter RJ. Cardioprotection and pharmacological therapies in acute myocardial infarction: Challenges in the current era. World J Cardiol 2014; 6:100-106.
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25. Zhang M-q, Zheng Y-l, Chen H, Tu J-f, Shen Y, Guo J-p, et al. Sodium tanshinone IIA sulfonate protects rat myocardium against ischemia-reperfusion injury via activation of PI3K/Akt/FOXO3A/Bim pathway. Acta Pharmacol Sin 2013; 34:1386-1396.
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26. Bagai A, Dangas GD, Stone GW, Granger CB. Reperfusion strategies in acute coronary syndromes. Circ Res 2014;114:1918-1928.
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35. Yu Q, Chen H, Sheng L, Liang Y, Li Q. Sodium tanshinone IIA sulfonate prolongs the survival of skin allografts by inhibiting inflammatory cell infiltration and T cell proliferation. Int Immunopharmacol 2014; 22: 277-284.
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36. Sun N, Li E, Wang Z, Zhao J, Wang S, He J, et al. Sodium tanshinone IIA sulfonate inhibits porcine reproductive and respiratory syndrome virus via suppressing N gene expression and blocking virus-induced apoptosis. Antivir Ther 2014; 19:89-95.
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37. Liu HC, Liu HH. [Adverse reactions of tanshinone II(A) sodium sulfonate injection in treating 18 cases: an analysis of clinical features]. Zhongguo Zhong Xi Yi Jie He Za Zhi 2013; 33:1287-1289.
37
ORIGINAL_ARTICLE
Cinnamaldehyde and eugenol change the expression folds of AKT1 and DKC1 genes and decrease the telomere length of human adipose-derived stem cells (hASCs): An experimental and in silico study
Objective(s): To investigate the effect of cinnamaldehyde and eugenol on the telomere-dependent senescence of stem cells. In addition, to search the probable targets of mentioned phytochemicals between human telomere interacting proteins (TIPs) using in silico studies. Materials and Methods: Human adipose derived stem cells (hASCs) were studied under treatments with 2.5 µM/ml cinnamaldehyde, 0.1 µg/ml eugenol, 0.01% DMSO or any additive. The expression of TERT, AKT1 and DKC1 genes and the telomere length were assessed over 48-hr treatment. In addition, docking study was conducted to show probable ways through which phytochemicals interact with TIPs. Results: Treated and untreated hASCs had undetectable TERT expression, but they did affect the AKT1 and DKC1 expression levels (CI=0.95; P<0.05). The telomere lengths reduced in phytochemicals treated with hASCs when compared with the untreated cells (P<0.05). Docking results showed that the TIPs might be the proper targets for cinnamaldehyde and eugenol. Data mining showed there are many targets for cinnamaldehyde and eugenol in the intracellular environment. Conclusion: The general effect of cinnamaldehyde and eugenol is their induction of stem cell senescence. Therefore, they could be applicable as chemo-preventive or antineoplastic agents.
https://ijbms.mums.ac.ir/article_8362_70d7e96d3cd96ed5607f33aef067bab7.pdf
2017-03-01
316
326
10.22038/ijbms.2017.8362
Aging
Cinnamaldehyde
Eugenol
Stem cells
Telomerase
Telomere
Abdorrahim
Absalan
abdorrahim.absalan@modares.ac.ir
1
Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Seyed Alireza
Mesbah-Namin
mesbahna@modares.ac.ir
2
Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
LEAD_AUTHOR
Taki
Tiraihi
ttiraihi@gmail.com
3
Department of Anatomical Sciences, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Taher
Taheri
tahertaheri@irimc.org
4
Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran
AUTHOR
1. Flores I, Blasco MA. The role of telomeres and telomerase in stem cell aging. FEBS Lett 2010; 584:3826-3830.
1
2. Wong C-C, Li H-B, Cheng K-W, Chen F. A systematic survey of antioxidant activity of 30 Chinese medicinal plants using the ferric reducing antioxidant power assay. Food Chem 2006; 97:705-711.
2
3. Zaveri NT. Green tea and its polyphenolic catechins: Medicinal uses in cancer and noncancer applications. Life Sci 2006; 78:2073-2080.
3
4. Ho YS, So KF, Chang RCC. Anti-aging herbal medicine—How and why can they be used in aging-associated neurodegenerative diseases? Ageing Res Rev 2010; 9:354-362.
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5. Ogata M, Hoshi M, Urano S, Endo T. Antioxidant activity of eugenol and related monomeric and dimeric compounds. Chem Pharm Bull 2000; 48:1467-1469.
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6. Fang SH, Rao YK, Tzeng YM. Cytotoxic effect of trans-cinnamaldehyde from cinnamomum osmo-phloeum leaves on Human cancer cell lines. Int J Appl Sci Eng 2004; 2:136-147.
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7. Jaganathan SK, Mazumdar A, Mondhe D, Mandal M. Apoptotic effect of eugenol in human colon cancer cell lines. Cell Biol Int 2011; 35:607-15.
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8. Chuang LY, Guh JY, Chao LK, Lu YC, Hwang JY, Yang YL, et al. Anti-proliferative effects of cinnamaldehyde on human hepatoma cell lines. Food Chem 2012; 133:1603-1610.
8
9. King AA, Shaughnessy DT, Mure K, Leszczynska J, Ward WO, Umbach DM, et al. Antimutagenicity of cinnamaldehyde and vanillin in human cells: Global gene expression and possible role of DNA damage and repair. Mutat Res 2007; 616:60-69.
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10. Chao LK, Hua KF, Hsu HY, Cheng SS, Lin IF, Chen CJ, et al. Cinnamaldehyde inhibits pro-inflammatory cytokines secretion from monocytes/macrophages through suppression of intracellular signaling. Food Chem Toxicol 2008; 46:220-231.
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11. Tao G, Irie Y, Li D-J, Keung WM. Eugenol and its structural analogs inhibit monoamine oxidase A and exhibit antidepressant-like activity. Bioorgan Med Chem 2005; 13:4777-47788.
11
12. Absalan A, Mesbah-Namin SA, Tiraihi T, Taheri T. The effects of cinnamaldehyde and eugenol on human adipose-derived mesenchymal stem cells viability, growth and differentiation: a cheminformatics and in vitro study. Avicenna J Phytomed 2016; 1-11.
12
13. Dokal I. Dyskeratosis congenita. Hematology Am Soc Hematol Educ Program 201; 1:480-486.
13
14. Plunkett FJ, Franzese O, Finney HM, Fletcher JM, Belaramani LL, Salmon M, et al. The loss of telomerase activity in highly differentiated CD8+CD28-CD27- T cells is associated with decreased Akt (Ser473) phosphorylation. J Immunol 2007; 178:7710-7719.
14
15. Kuzuhara T, Suganuma M, Fujiki H. Green tea catechin as a chemical chaperone in cancer prevention. Cancer Lett 2008; 261:12-20.
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16. Aggarwal S, Ichikawa H, Takada Y, Sandur SK, Shishodia S, Aggarwal BB. Curcumin (diferuloylmethane) down-regulates expression of cell proliferation and antiapoptotic and metastatic gene products through suppression of IκBα kinase and Akt activation. Mol Pharmacol 2006; 69:195-206.
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17. O’Callaghan NJ, Fenech M. A quantitative PCR method for measuring absolute telomere length. Biol Proced Online 2011; 13:1-10.
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18. Podlevsky JD, Bley CJ, Omana RV, Qi X, Chen JJ. The telomerase database. Nucleic Acids Res 2008; 36:D339-D343.
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19. Kiefer F, Arnold K, Künzli M, Bordoli L, Schwede T. The SWISS-MODEL Repository and associated resources. Nucleic Acids Res 2009; 37: D387-D92.
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20. Arnold K, Bordoli L, Kopp J, Schwede T. The SWISS-MODEL Workspace: A web-based environment for protein structure homology modelling. Bioinformatics 2006; 22:195-201.
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21. Irwin JJ, Shoichet BK. ZINC-a free database of commercially available compounds for virtual screening. J Chem Inf Model 2005; 45:177-182.
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22. Thomsen R, Christensen MH. MolDock: a new technique for high-accuracy molecular docking. J Med Chem 2006; 49:3315-3321.
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23. Franceschini A, Szklarczyk D, Frankild S, Kuhn M, Simonovic M, Roth A, et al. STRING v9.1: protein-protein interaction networks, with increased coverage and integration. Nucleic Acids Res 2013; 41:D808-815.
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24. Zimmermann S, Voss M, Kaiser S, Kapp U, Waller CF, Martens UM. Lack of telomerase activity in human mesenchymal stem cells. Leukemia 2003; 17:1146-1149.
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25. Python F, Goebel C, Aeby P. Comparative DNA microarray analysis of human monocyte derived dendritic cells and MUTZ-3 cells exposed to the moderate skin sensitizer cinnamaldehyde. Toxicol Appl Pharmacol 2009; 239:273-283.
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26. Aviv A, Hunt SC, Lin J, Cao X, Kimura M, Blackburn E. Impartial comparative analysis of measurement of leukocyte telomere length/DNA content by Southern blots and qPCR. Nucleic Acids Res 2011; 39:e134.
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27. Murakami A, Ohnishi K. Mechanisms underlying food functionality via molecular chaperones: chemical training hypothesis. J Food Drug Anal 2012; 20:257-260.
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28. Grover A, Shandilya A, Agrawal V, Pratik P, Bhasme D, Bisaria VS, et al. Hsp90/Cdc37 Chaperone/co-chaperone complex, a novel junction anticancer target elucidated by the mode of action of herbal drug Withaferin A. BMC Bioinformatics 2011; 12:S30.
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29. Gruber JV, Holtz R. Examining the genomic influence of skin antioxidants in vitro. Mediat Inflamm 2010; 2010. pii: 230450.
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32. Strati A, Papoutsi Z, Lianidou E, Moutsatsou P. Effect of ellagic acid on the expression of human telomerase reverse transcriptase (hTERT) α+ β+ transcript in estrogen receptor-positive MCF-7 breast cancer cells. Clin Biochem 2009; 42:1358-1362.
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34. Blackburn EH. Switching and signaling at the telomere. Cell 2001; 106:661-673.
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36. Fiset S, Chabot B. hnRNP A1 may interact simultaneously with telomeric DNA and the human telomerase RNA in vitro. Nucleic Acids Res 2001; 29:2268-2275.
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41. Zhang JH, Liu LQ, He YL, Kong WJ, Huang SA. Cytotoxic effect of trans-cinnamaldehyde on human leukemia K562 cells. Acta Pharmacol Sin 2010; 31:861-866.
41
ORIGINAL_ARTICLE
Selection of single-chain variable fragments specific for Mycobacterium tuberculosis ESAT-6 antigen using ribosome display
Objective(s): Tuberculosis (TB) is still one of the problematic infectious diseases in developing countries, especially in Iran. In the present study, we applied ribosome display technique to select single chain variable fragments (scFvs) specific for the 6-kDa early secretory antigenic target (ESAT-6) antigen of Mycobacterium tuberculosis from a mouse scFv library. Materials and Methods: The gene encoding ESAT-6 was cloned into pET22b(+) plasmid and expressed in Escherichia coli BL21 (DE3). The purified recombinant ESAT-6 protein was injected into female BALB/c mice for immunization, and then m-RNA was extracted from the spleen of immunized mice. The anti-ESAT-6 VH/k chain library was assembled by joining of VH and k into the VH/k chain with a 72-bp DNA linker by SOE (splicing by overlap extension) PCR. The scFv library was panned against ESAT-6 using a single round of ribosome display via a rabbit reticulocyte lysate system. Results: ELISA assay showed that one of the selected scFvs had higher affinity against the recombinant ESAT-6 protein. The affinity of the candidate scFv was ̴ 3.74×108 M-1. Conclusion: It could be proposed that the isolated scFv in this study may be useful for the diagnosis of TB.
https://ijbms.mums.ac.ir/article_8363_16ac0a55e10a7d3e325be59b8f336354.pdf
2017-03-01
327
333
10.22038/ijbms.2017.8363
antibody
ESAT-6
Mycobacterium tuberculosis
Ribosome display
scFv
Shahrzad
Ahangarzadeh
shahrzadahangar@yahoo.com
1
Department of Biotechnology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mojgan
Bandehpour
bandehpour@gmail.com
2
Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Bahram
Kazemi
bahram_14@yahoo.com
3
Department of Biotechnology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
1. Zumla A, George A, Sharma V, Herbert RH, Baroness Masham of I, Oxley A, et al. The WHO 2014 global tuberculosis report--further to go. Lancet Glob Health. 2015; 3:e10-2.
1
2. Getahun H, Harrington M, O'Brien R, Nunn P. Diagnosis of smear-negative pulmonary tuberculosis in people with HIV infection or AIDS in resource-constrained settings: informing urgent policy changes. Lancet 2007; 369:2042-2049.
2
3. Mukundan H, Kumar S, Price DN, Ray SM, Lee YJ, Min S, et al. Rapid detection of Mycobacterium tuberculosis biomarkers in a sandwich immunoassay format using a waveguide-based optical biosensor. Tuberculosis (Edinb) 2012; 92:407-416.
3
4. van Ingen J, de Zwaan R, Dekhuijzen R, Boeree M, van Soolingen D. Region of difference 1 in nontuberculous Mycobacterium species adds a phylogenetic and taxonomical character. J Bacteriol 2009; 191:5865-5867.
4
5. Ganguly N, Giang PH, Gupta C, Basu SK, Siddiqui I, Salunke DM, et al. Mycobacterium tuberculosis secretory proteins CFP-10, ESAT-6 and the CFP10:ESAT6 complex inhibit lipopolysaccharide-induced NF-kappaB transactivation by downregulation of reactive oxidative species (ROS) production. Immunol Cell Biol 2008; 86:98-106.
5
6. van Pinxteren LA, Ravn P, Agger EM, Pollock J, Andersen P. Diagnosis of tuberculosis based on the two specific antigens ESAT-6 and CFP10. Clin Diagn Lab Immunol 2000; 7:155-160.
6
7. Brodin P, de Jonge MI, Majlessi L, Leclerc C, Nilges M, Cole ST, et al. Functional analysis of early secreted antigenic target-6, the dominant T-cell antigen of Mycobacterium tuberculosis, reveals key residues involved in secretion, complex formation, virulence, and immunogenicity. J Biol Chem 2005; 280:33953-33959.
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8. Ahmad ZA, Yeap SK, Ali AM, Ho WY, Alitheen NB, Hamid M. scFv antibody: principles and clinical application. Clin Dev Immunol 2012; 2012:980250.
8
9. Nelson AL. Antibody fragments: hope and hype. MAbs 2010; 277-83.
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10. Gan R, Jewett MC. Evolution of translation initiation sequences using in vitro yeast ribosome display. Biotechnol Bioeng 2016; 113:1777-1786.
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11. Holliger P, Hudson PJ. Engineered antibody fragments and the rise of single domains. Nat Biotechnol 2005; 23:1126-1136.
11
12. He M, Taussig MJ. Ribosome display of antibodies: expression, specificity and recovery in a eukaryotic system. J Immunol Methods 2005; 297:73-82.
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13. Weichhart T, Horky M, Sollner J, Gangl S, Henics T, Nagy E, et al. Functional selection of vaccine candidate peptides from Staphylococcus aureus whole-genome expression libraries in vitro. Infect Immun 2003; 71:4633-4641.
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14. Hanes J, Pluckthun A. In vitro selection and evolution of functional proteins by using ribosome display. Proc Natl Acad Sci U S A 1997; 94:4937-4942.
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15. Mattheakis LC, Bhatt RR, Dower WJ. An in vitro polysome display system for identifying ligands from very large peptide libraries. Proc Natl Acad Sci U S A 1994; 91:9022-9026.
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16. Pluckthun A. Ribosome display: a perspective. Methods Mol Biol 2012; 805:3-28.
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17. Binz HK, Amstutz P, Kohl A, Stumpp MT, Briand C, Forrer P, et al. High-affinity binders selected from designed ankyrin repeat protein libraries. Nat Biotechnol 2004; 22:575-582.
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18. He M, Taussig MJ. Antibody-ribosome-mRNA (ARM) complexes as efficient selection particles for in vitro display and evolution of antibody combining sites. Nucleic Acids Res 1997; 25:5132-5134.
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19. Zhou L, Mao WP, Fen J, Liu HY, Wei CJ, Li WX, et al. Selection of scFvs specific for the HepG2 cell line using ribosome display. J Biosci 2009; 34:221-226.
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ORIGINAL_ARTICLE
Protective effect of Crocus sativus L. (Saffron) extract on spinal cord ischemia-reperfusion injury in rats
Objective(s): Ischemia/reperfusion (I/R) injury of spinal cord is leading to the paraplegia observed. In this study, we investigated the protective effect of the saffron extract on spinal cord I/R injury. Materials and Methods: Thirty five male Sprague-Dawley rats were divided into 5 groups: intact, sham surgery, normal saline (NS), low dose saffron aqua extract, high dose saffron aqua extract. Results: The mean motor deficit index (MDI) scores were significantly lower in the saffron extract groups than in the NS group at 48 hr after spinal cord ischemia (P<0.001). Saffron extract groups significantly decreased plasma level of malondialdehyde than in the NS Group (P<0.05). The number of motor normal neurons was significantly greater in the high saffron extract group than in the NS and low saffron group (P<0.05). Conclusion: These data suggest that a saffron extract may protect spinal cord neurons from I/R injury.
https://ijbms.mums.ac.ir/article_8364_b85d5b5c30289647718f2d695bde1869.pdf
2017-03-01
334
337
10.22038/ijbms.2017.8364
Ischemia
Reperfusion
Spinal Cord
Saffron extract
Gholam Hossein
Farjah
mdolatkhah@hotmail.com
1
Neurophysiology Research Center, Department of Anatomy, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
LEAD_AUTHOR
Shadi
Salehi
2
Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Mohammad Hasan
Ansari
sh12fm2@hotmail.com
3
Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Bagher
Pourheidar
4
Neurophysiology Research Center, Department of Anatomy, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
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