ORIGINAL_ARTICLE
Protective effect of silymarin against chemical-induced cardiotoxicity
Cardiac disorders remain one of the most important causes of death in the world. Oxidative stress has been suggested as one of the molecular mechanisms involved in drug-induced cardiac toxicity. Recently, several natural products have been utilized in different studies with the aim to protect the progression of oxidative stress-induced cardiac disorders. There is a large body of evidence that administration of antioxidants may be useful in ameliorating cardiac toxicity. Silymarin, a polyphenolic flavonoid has been shown to have utility in several cardiovascular disorders. In this review, various studies in scientific databases regarding the preventive effects of silymarin against cardiotoxicity induced by chemicals were introduced. Although there are many studies representing the valuable effects of silymarin in different diseases, the number of researches relating to the possible cardiac protective effects of silymarin against drugs induced toxicity is rather limited. Results of these studies show that silymarin has a broad spectrum of cardiac protective activity against toxicity induced by some chemicals including metals, environmental pollutants, oxidative agents and anticancer drugs. Further studies are needed to establish the utility of silymarin in protection against cardiac toxicity.
https://ijbms.mums.ac.ir/article_7590_84dc813159e5eff60d9cd251d6fe7982.pdf
2016-09-01
916
923
10.22038/ijbms.2016.7590
Cardiotoxicity
Metals
Oxidative stress
Silybum marianum
Silymarin
Bibi Marjan
Razavi
1
Targeted Drug Delivery Research Center, Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Gholamreza
Karimi
karimigh@mums.ac.ir
2
Pharmaceutical Research Center, Pharmacy School, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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60
ORIGINAL_ARTICLE
Association of morphine-induced analgesic tolerance with changes in gene expression of GluN1 and MOR1 in rat spinal cord and midbrain
Objective(s): We aimed to examine association of gene expression of MOR1 and GluN1 at mRNA level in the lumbosacral cord and midbrain with morphine tolerance in male Wistar rats. Materials and Methods: Analgesic effects of morphine administrated intraperitoneally at doses of 0.1, 1, 5 and 10 mg/kg were examined using a hot plate test in rats with and without a history of 15 days morphine (10 mg/kg) treatment. Morphine-induced analgesic tolerance was also assessed on days 1, 5, 10 and 15 of chronic morphine injections. Two groups with history of 15 days injections of saline or morphine (10 mg/kg) were decapitated on day 15 and their lumbosacral cord and midbrain were dissected for evaluating MOR1 and GluN1 gene expression. Results: The results of the hot plate test showed that morphine (5 and 10 mg/kg) induced significant analgesia in naïve rats but its analgesic effects in rats receiving 15 days injections of morphine (10 mg/kg) was decreased, indicating tolerance to morphine analgesia. The results also showed that the GluN1 gene expression in tolerant rats was decreased by 71 % in the lumbosacral cord but increased by 110 % in the midbrain compared to the control group. However, no significant change was observed for the MOR1 gene expression in both areas. Conclusion: It can be concluded that tolerance following administration of morphine (10 mg/kg) for 15 days is associated with site specific changes in the GluN1 gene expression in the spinal cord and midbrain but the MOR1 gene expression is not affected.
https://ijbms.mums.ac.ir/article_7591_d52a6c65b173b8d0acb89b969d3eb126.pdf
2016-09-01
924
931
10.22038/ijbms.2016.7591
Analgesic tolerance
Gene expression
Mu-opioid receptor
NMDA receptor
Rat
Shamseddin
Ahmadi
shamseddin2000@yahoo.com
1
Department of Biological Science, Faculty of Science, University of Kurdistan, Sanandaj, Iran
LEAD_AUTHOR
Fatemeh
Miraki
fateme.miraki@yahoo.com
2
Department of Biological Science, Faculty of Science, University of Kurdistan, Sanandaj, Iran
AUTHOR
Jalal
Rostamzadeh
j.rostamzadeh@uok.ac.ir
3
Department of Biological Science, Faculty of Science, University of Kurdistan, Sanandaj, Iran
AUTHOR
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48
ORIGINAL_ARTICLE
The effect of oral and intraurethral trimetazidine use on urethral healing
Objective(s): We aimed to study the effect of trimetazidine (TMZ) on urethral wound repair.
Materials and Methods: A total of 52 male rats were used; 8 groups were formed: 1-week and 3-week control (C1,C3), sham (S1, S3), oral (OT1, OT3), and intraurethral TMZ (IUT1, IUT3) groups. Serum and urine total antioxidant capacity (TAC), total oxidant capacity (TOC), and 8-hydroxy-deoxy-guanosine (8-OHdG) were studied. Hematoxyline-Eosin was used for the histopathological study. In addition, tumor necrosis factor alpha (TNF- α), interleukin 1α, and β levels were compared across groups by an immunohistochemical method.
Results: There were significant differences between C3 and IUT3, OT3 and IUT3 with respect to serum TAC in 3-week groups (P=0.013; P =0.001). Serum TOC levels were significantly different between C3 and IUT3; S3 and OT3; and OT3 and IUT3 groups (P =0.024; P =0.019; P =0.000, respectively). Serum 8-OHdG levels were significantly different between C3 and OT3 groups (P=0.033). In the immunohistochemical examination, C1 and OT1; C1 and IUT1; and S1, S3, OT1, OT3, IUT1 groups were significantly different with respect to IL-1β staining (P=0.007; P =0.000; P=0.009), while there was a significant difference between C3 and S3 with respect to IL-1β (P =0.000).
Conclusion: TMZ increased urinary total oxidant level; while increasing serum TAC levels in the long-term. It also reduced serum TAC levels in urethral use and caused an increase in serum TOC levels with minimal effects on DNA injury and repair. No effect was detected on IL1 α and TNF, but partially reduced the effect on IL-1 β levels.
https://ijbms.mums.ac.ir/article_7592_dd2ecf4a40f637ea35f5d633f431c69b.pdf
2016-09-01
932
939
10.22038/ijbms.2016.7592
Oxidative stress
Trimetazidine
Urethral healing
Urethral Injury
Ali
Ayyildiz
urology52@gmail.com
1
Ordu University Medical Faculty, Urology Department, Ordu, Turkey
LEAD_AUTHOR
Sema Nur
Ayyildiz
2
Ordu University Medical Faculty, Clinical Biochemistry Department, Ordu, Turkey
AUTHOR
Erdal
Benli
drerdalbenli@gmail.com
3
Ordu University Medical Faculty, Urology Department, Ordu, Turkey
AUTHOR
Havva
Erdem
4
Ordu University Medical Faculty, Pathology Department, Ordu, Turkey
AUTHOR
Selma
Cirrik
5
Ordu University Medical Faculty, Pathology Department, Ordu, Turkey
AUTHOR
Tevfik
Noyan
6
Ordu University Medical Faculty, Clinical Biochemistry Department, Ordu, Turkey
AUTHOR
R. Cankon
Germiyanoglu
7
Ondokuz Mayıs University Medical Faculty, Urology Department, Samsun, Turkey
AUTHOR
Abdullah
Çirakoglu
8
Ordu University Medical Faculty, Urology Department, Ordu, Turkey
AUTHOR
1. Ayyıldız A, Akgül K.T, Cebeci Ö, Nuhoğlu B, Caydere M, Ustün H, et al. Intraurethral honey application for urethral injury: an experimental study. Int Urol Nephrol 2007; 39: 815-821.
1
2. Ayyıldız A, Nuhoglu B, Gülerkaya B, Caydere M, Ustün H, Germiyanoglu C, et al. Effect of intraurethral Mitomycin-C on healing and fibrosis in rats with experimentally induced urethral stricture. Int J Urol 2004; 11: 1122-1126.
2
3. Parihar A, Parihar MS, Milner S, Bhat S. Oxidative stres and antioksidative mobilization in burn injury. Burns 2008; 34: 6-17.
3
4. Aksoy H, Özakpınar ÖB. Yara iyileşmesi ve oksidatif stres. Marmara Pharm J 2014; 18: 153-158.
4
5. Sucu S, Unlu A, Tamer L, Aytacoğlu B, Coskun B, Bilgin R, et al. Effects of trimetazidine on tissue damage in kidney after hindlimb ischemia-reperfusion. Pharmacol Res 2002; 46:345-349.
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6. Harpey C, Clauser P, Labrid C, Freyria JL, Poirier JP. Trimetazidine, a cellular anti-ischemic agent. Cardiovasc Drug Rev 1988; 6:292–312.
6
7. Hauet Th, Bauza G, Goujon M, Caritez JC, Carretier M, Eugene M, et al. Effects of trimetazidine on lipid peroxidation and phosphorous metabolites during cold storage and reperfusion of isolated perfused rat kidney. Pharmacol Exp Ther 1998; 285:1061-1067.
7
8. Williams FM, Tanda K, Kus M, Williams TJ. Trimetazidine inhibits neutrophil accumulation after myocardial ischemia and reperfusion in rabbits. J Cardiovasc Pharmacol 1993; 22:828-833.
8
9. Erel O. A novel automated method to measure total antioxidant response againts potent free radical reactions. Clin Biochem 2004; 37:112-119.
9
10. Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem 2005; 38:1103-1111.
10
11. Ninan N, Thomas S, Grohens Y. Wound healing in urology. Adv Drug Deliv Rev 2015; 82-83:93-105.
11
12. Kumar S, Wong PF, Leaper DJ. What is new wound healing? Turk J Med Sci 2004; 34:147-160.
12
13. Yalcinkaya FR, Davarci M, Gokce A, Güven EO, İnci M, Kerem M, et al. Intraurethral utterbasti application for urethral injury in rats. J Anim Vet Adv 2002; 11:1494-1497.
13
14. Carden DL, Granger DN. Pathophysiology of ischemia-reperfusion injury. J Pathol 2000; 190:255-266.
14
15. Cross HR. Trimetazidine: a novel protective role via maintenance of Na+-K+ ATPase activity? Cardiovasc Res 2000; 47:637-639.
15
16. Granger DN. Role of xanthine oxidase and granulocytes in ischemia-reperfusion injury. Am J Physiol 1988; 255:1269-1275.
16
17. Wu Q, Qi B, Liu Y. Mechanisms underlying protective effects of trimetazidine on endothelial progenitor cells biological functions against H2O2-induced injury: involvement of antioxidation and Akt/eNOS signaling pathways. Eur J Pharmacol 2013; 707:87-94.
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18. Kuralay F, Çavdar Z. İnflamatuar medyatörlere toplu bakış. Genel Tıp Derg 2006; 16:143-152.
18
19. Hofer MD, Cheng EY, Bury MI, Park E, Xu W, Hong SJ, et al. Analysis of primary urethral wound healing in the rat. Urology 2014; 84:246. e241-e247
19
ORIGINAL_ARTICLE
Apoptosis induction of human endometriotic epithelial and stromal cells by noscapine
Objective(s): Endometriosis is a complex gynecologic disease with unknown etiology. Noscapine has been introduced as a cancer cell suppressor. Endometriosis was considered as a cancer like disorder, The aim of present study was to investigate noscapine apoptotic effect on human endometriotic epithelial and stromal cells in vitro. Materials and Methods:In this in vitro study, endometrial biopsies from endometriosis patients (n=9) were prepared and digested by an enzymatic method (collagenase I, 2 mg/ml). Stromal and epithelial cells were separated by sequential filtration through a cell strainer and ficoll layering. The cells of each sample were divided into five groups: control (0), 10, 25, 50 and 100 micromole/liter (µM) concentration of noscapine and were cultured for three different periods of times; 24, 48 and 72 hr. Cell viability was assessed by colorimetric assay. Nitric oxide (NO) concentration was measured by Griess reagent. Cell death was analyzed by Acridine Orange (AO)–Ethidium Bromide (EB) double staining and Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay. Data were analyzed by one-way ANOVA. Results: Viability of endometrial epithelial and stromal cells significantly decreased in 10, 25, 50 and 100 µM noscapine concentration in 24, 48, 72 hr (P<0.05) and apoptotic index increased in 25, 50 and 100 µM noscapine concentrations in 48 hr significantly (P<0.05). Concentrations of NO didn’t show a significant decrease. Conclusion: Noscapine increased endometriotic epithelial and stromal cell death and can be suggested as a treatment for endometriosis.
https://ijbms.mums.ac.ir/article_7593_97828c0e9a36e5e338fc90db08a982c5.pdf
2016-09-01
940
945
10.22038/ijbms.2016.7593
Apoptosis
Endometriosis
Nitric oxide
Noscapine
Mohammad Rasoul
Khazaei
mrasoolkhazaei@gmail.com
1
Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Zahra
Rashidi
rashidi.zahra@gmail.com
2
Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Farzaneh
Chobsaz
3
Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Mozafar
Khazaei
mkhazaei134@yahoo.com
4
Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
LEAD_AUTHOR
1. Dunselman GA, Vermeulen N, Becker C, Calhaz-Jorge C, D'Hooghe T, De Bie B, et al ESHRE guideline: management of women with endometriosis. European Society of Human Reproduction and Embryology. Hum Reprod 2014; 29:400-412.
1
2. Vignali M, Infantino M, Matronem R, Chiodo I, Somigliana E, Busacca M, et al Endometriosis: novel etiopathogenetic concepts and clinical perspectives. Fertil Steril 2002; 78; 665–678.
2
3. Nap AW, Groothuis PG, Demir AY, Evers JL, Dunselman GA. Pathogenesis of endometriosis. Best Practice and Research Clinical Obstetrics and Gynaecolgy 2004; 18: 233–244.
3
4. Giudice LC, Kao LC. Endometriosis. Lancet 2004; 364:1789-1799.
4
5. Yadav L, Puri N, Rastogi V, Satpute P, Sharma V. Tumour Angiogenesis and Angiogenic Inhibitors: A Review. J Clin Diagn Res. 2015; 9: XE01–XE05.
5
6. Taylor RN, Lebovic DI. Mueller MD. Angiogenic factors in endometriosis. Annals of New York Academy Sciences 2002; 955; 89-100.
6
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8. Huang HY. Medical Treatment of Endometriosis. Chang Gung Med J. 2008; 31: 431-440.
8
9. Vercellini P, De Giorgi O, Mosconi P, Stellato, G, Vicentini S, Crosignani PG. Cyproterone acetate versus a continuous monophasic oral contraceptive in the treatment of recurrent pelvic pain after conservative surgery for symptomatic endometriosis. Fertil Steril 2002; 77: 52- 61.
9
10. Kettel LM, Murphy AA, Morales AJ, Yen SS. Preliminary report on the treatment of endometriosis with low-dos mifepristone (RU 486). Am J Obstet Gynecol 1998; 178: 1151-1156.
10
11. Esfandiari N, Khazaei M, Jafar A, Bielecki R, Gotlieb L, Ryan E. et al Effect of a statin on an in vitro model of endometriosis. Fertil Steril 2007; 87: 257–262.
11
12. Rezavand N, Khazaei M, Oliapanah E, Nikzad H, Khazaei MR. Low doses of celecoxib stimulate human endometrium growth in a three-dimensional culture model. Int J Fertil Steril 2013; 7: 7-12.
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13. Kokawa K, Shikone T, Nakano R. Apoptosis in the human uterine endometrium during the menstrual cycle. J Clinic Endocrin Met 1996; 81: 4144-4147.
13
14. Meresman GF, Bilotas MA, Lombardi E, Tesone M, Sueldo C, Baranao R. Effect of GnRH analogues on apoptosis and release of interleukin-1b and vascular endothelial growth factor in endometrial cell cultures from patients with endometriosis. Hum Reprod 2003; 18: 1767-1771.
14
15. Mahmoudian M. Recent progress in clinical application of noscapine: a review. Cur Topics Pharmacology 2006; 10: 81-86.
15
16. Ebrahimi SA, Zareie-Rostami P, Mahmoudian M. Interaction of noscapine with the bradukinin mediation of cough response. Acta Physiolo 2003; 90: 147-155.
16
17- Landen JW, Lang R, McMahon SJ, Rusan NM, Yvon AM, Adams AW, et al Noscapine alters microtubule dynamics in living cells and inhibits the progression of melanoma. Cancer Research 2002; 62: 4109-4114.
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18. Aneja R, Ghaleb AM, Zhou J, Yang VW. Joshi HC. P53 and p21 determine the sensitivity of noscapine-induced apoptosis in colon cancer cells. Cancer Research 2007; 67: 3862-3870.
18
19. Ye K, Ke Y, Keshava N, Shanks J, Kapp JA, Tekmal RR, et al Opium alkaloid noscapine is an antitumor agent that arrest metaphase and induces apoptosis in dividing cells. Proceeding of the National Academy of Sciences USA 1998; 95: 1601-1606.
19
20- Mahmoudian M. Rahimi-Moghaddam P. The anti-cancer activity of noscapine: a review. Recent Patents on Anticancer Drug Discovery 2009; 4: 92-97.
20
21. Barken I, Geller J, Rogosnitzky M. Noscapine inhibits human prostate cancer progression and metastasis in a mouse model. Anticancer Research 2008; 28: 3701-3704.
21
22. Khazaei M, Chobsaz F, Khazaei S. The effect of different doses of clomiphene citrate on morphology and proliferation of endometrial stromal cells in in-vitro culture. J Bab Uni Med Sci. 2010; 12: 7-12.
22
23. Tayarani-Najaran Z, Parsaee H, Hoseini A. Mousavi SH. Study of noscapine-induced cell death in hepatocellular carcinoma cell Line. Pharmacology online 2009; 3: 522-530.
23
24. Khazaei M, Roshankhah Sh, Ghorbani P. Chobsaz F. Sildenafil effect on nitric oxide secretion by normal human endometrial epithelial cells cultured in vitro. Int J Fertil Steril 2011; 5; 142-147.
24
25. Mirzapur P, Rashidi Z, Rezakhani L, Khazaei M. In vitro inhibitory effect of crab shell extract on human umbilical vein endothelial cell. In Vitro Cellular & Developmental Biology –Animal 2015; 51: 36-41.
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26. Baskic D, Popovic S, Ristic P, Nebojsa N. Analysis of cycloheximide-induced apoptosis in human leukocytes: Fluorescence microscopy using annexin V/propidium iodide versus acridin orange/ethidium bromide. Cell Biol Intern 2006; 30, 924-932.
26
27. Rashidi Z, Azadbakht M, Khazaei M. Hydrostatic pressure improves in-vitro maturation of oocytes derived from vitrified-warmed mouse ovaries. Iran J Reprod Med. 2012; 10: 257-64.
27
28. Chougule MB, Apurva RP, Jackson T, Patel R. Antitumor activity of noscapine in combination with doxorubicin in triple negative breast cancer. Mandip Singh PLoS ONE 2011; 3: 1-12.
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29. Ronald l Steve JM, Jaren W, McMahon J. Noscapine alters microtubule dynamics and inhibits the progression of melanoma in living cells. Cancer Res 2002; 62: 4109-4114.
29
30. Zhou J, Gupta K, Aggarwal S, Aneja R, Chandra R, Panda D, et al Brominated derivatives of noscapine are potent microtubule-interfering agents that perturb mitosis and inhibit cell proliferation. Molecular Pharmacology 2003; 63: 799-807.
30
31. Heidari N, Goliaei B, Moghaddam PR, Rahbar-Roshandel N, Mahmoudian M. Apoptotic pathway induced by noscapine in human myelogenous leukemic cells. Anticancer Drugs 2007; 18: 1139-1147.
31
32. Wu MY, Chao KH, Yang JH, Lee TH, Yang YS, Ho HN, Nitric oxide synthesis is increased in the endometrial tissue of women with endometriosis. Hum Reprod 2003; 18: 2668- 2671.
32
33. BakanE, Taysi S, Polat MF, Dalga Z, Bakan N, Gumus M. Nitric oxide levels and lipid peroxidation in plasma of patients with gastric cancer. Clinical Oncology 2002; 32:162-166.
33
34. Tong X. Li H. eNOS protects prostate cancer cells from TRAIL-induced apoptosis. Cancer Letters 2004; 210: 63–71.
34
35. Vaskivuo TE, Stenbäck F, Karhumaa P, Risteli J, Dunkel L. Tapanainen JS. Apoptosis and apoptosis-related proteins in human endometrium. Molecular Cellular Endocrinology 2000; 165: 75-83.
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36. Dahmoun M, Boman K, Cajander S, Westin P, Bäckström T. Apoptosis, proliferation and sex hormone receptors in superficial parts of human endometrium at the end of the secretory phase. J Clin Endocrinol Meta 1999; 84: 1737-1743.
36
37. Osborn BH, Haney AF, Misukonis MA, Weinberg JB. Inducible nitric oxide synthase expression by peritoneal macrophages in endometriosis-associated infertility. Fertil Steril 2002; 77: 46-51.
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38. Gebel HM, Braun DP, Tambur A, Frame D, Rana N, Dmowski WP. Spontaneous apoptosis of endometrial tissue is impaired in women with endometriosis. Fertil Steril 1998; 69: 1042-1047.
38
39. Dmowski WP, Ding J, Shen J, Rana N, Fernandez BB, Braun DP. Apoptosis in endometrial glandular and stromal cells in women with and without endometriosis. Hum Reprod 2001; 16: 1802-1808.
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40. Dunselman GA, Hendrix MG, Bouckaert PX, Evers JL. Functional aspects of peritoneal macrophages in endometriosis of women. J Reprod Fertil 1988; 82: 707-710.
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41. Fasciani A1, Bocci G, Xu J, Bielecki R, Greenblatt E, Leyland N, et al Three-dimensional in vitro culture of endometrial explants mimics the early stages of endometriosis. Fertil Steril. 2003; 80:1137-1143.
41
ORIGINAL_ARTICLE
Recognition and characterization of Erythropoietin binding-proteins in the brain of mice
Objective(s): Erythropoietin (EPO), is a 34KDa glycoprotein hormone, which belongs to type 1 cytokine superfamily. EPO involves in erythrocyte maturation through inhibition of apoptosis in erythroid cells. Besides its main function, protective effects of EPO in heart and brain tissues have been reported. EPO has a critical role in development, growth, and homeostasis of brain. Furthermore EPO has great potential in the recovery of different brain diseases which are still under studying. In this research, EPO binding pattern to brain proteins in animal model was studied. Materials and Methods:EPO antibody was covalently crosslinked to protein A/G agarose. in order to interact between EPO and its target in brain, about 5µg EPO added to brain homogenates(500ul of 1 mg/ml) and incubate at 4ο C for 30 min. brain tissue lysate were added to agarose beads, After isolation of target proteins(EPO - protein) both one and two-dimensional gel electrophoresis were performed. Proteins were identified utilizing MALDI-TOF/TOF and MASCOT software. Results: This research showed that EPO could physically interact with eightproteins including Tubulin beta, Actin cytoplasmic 2, T-complex protein 1, TPR and ankyrin repeat-containing protein 1, Centromere-associated protein E, Kinesin-like protein KIF7, Growth arrest-specific protein 2 and Pleckstrin homology-like domain family B member 2. Conclusion: Since EPO is a promising therapeutic drug for the treatment of neurological diseases, identified proteins may help us to have a better understanding about the mechanism of protective effects of EPO in the brain. Our data needs to be validated by complementary bioassays.
https://ijbms.mums.ac.ir/article_7594_3d898942bf5768f58e185238ea7fe692.pdf
2016-09-01
946
952
10.22038/ijbms.2016.7594
Brain
Erythropoietin
Immunoprecipitation
Proteomic screening
Target deconvolution
Neuroprotective effect
Reza
Kowsari
kowsarir@mums.ac.ir
1
Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Rezvan
Yazdian-Robati
yazdianr921@gmail.com
2
Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Bibi Marjan
Razavi
razavimr@mums.ac.ir
3
Targeted Drug Delivery Research Center, Department of Pharmacodinamy and Toxicology, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Atena
Pourtaji
pourtajia901@mums.ac.ir
4
Pharmaceutical Research Center, Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Maryam
Ghorbani
ghorbanim@gmail.com
5
Department of Pharmacology and Toxicology, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Hediye
Moghadam-Omranipour
moghadamm88@mums.ac.ir
6
Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hossein
Hosseinzadeh
hoseinzadehh@mums.ac.ir
7
Pharmaceutical Research Center, Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Parisa
Lari
larip881@mums.ac.ir
8
Pharmaceutical Research Center, Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Khalil
Abnous
abnouskh@mums.ac.ir
9
Pharmaceutical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
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4. Celik M, Gokmen N, Erbayraktar S, Akhisaroglu M, Konakc S, Ulukus C, et al. Erythropoietin prevents motor neuron apoptosis and neurologic disability in experimental spinal cord ischemic injury. Proc Natl Acad Sci U S A. 2002;99:2258-2263.
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8.Villa P, Bigini P, Mennini T, Agnello D, Laragione T, Cagnotto A, et al. Erythropoietin selectively attenuates cytokine production and inflammation in cerebral ischemia by targeting neuronal apoptosis. J Exp Med. 2003;198:971-975.
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9.Chen ZY, Asavaritikrai P, Prchal JT, Noguchi CT. Endogenous erythropoietin signaling is required for normal neural progenitor cell proliferation. J Biol Chem. 2007;282:25875-25883.
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10.Raida M. Drug target deconvolution by chemicalproteomics.Curr.Opin.Chem.Biol. 2011;15:570-575.
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11.Kajta Mg. Apoptosis in the central nervous system: mechanisms and protective strategies. Pol J Pharmacol. 2004;56:689-700.
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21.Gourlay CW, Ayscough KR. Identification of an upstream regulatory pathway controlling actin-mediated apoptosis in yeast. J. Cell Sci.. 2005;118:2119-2132.
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23.Merched A, Serot J-M, Visvikis S, Aguillon D, Faure G, Siest G. Apolipoprotein E, transthyretin and actin in the CSF of Alzheimer's patients: relation with the senile plaques and cytoskeleton biochemistry. Febs letters. 1998;425:225-228.
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24.Mosavi LK, Cammett TJ, Desrosiers DC, Peng Zy. The ankyrin repeat as molecular architecture for protein recognition. Protein Sci.2004;13:1435-1448.
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25.Main ER, Jackson SE, Regan L. The folding and design of repeat proteins: reaching a consensus. Curr Opin Struc Biol. 2003;13:482-9.
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26.Hirokawa N, Noda Y. Intracellular transport and kinesin superfamily proteins, KIFs: structure, function, and dynamics. Physiol Rev. 2008;88:1089-118.
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27.Dafinger C, Liebau MC, Elsayed SM, Hellenbroich Y, Boltshauser E, Korenke GC, et al. Mutations in KIF7 link Joubert syndrome with Sonic Hedgehog signaling and microtubule dynamics. J Clin Invest. 2011;121:2662-7.
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29.Marie SK, Okamoto OK, Uno M, Hasegawa APG, Oba‐Shinjo SM, Cohen T, et al. Maternal embryonic leucine zipper kinase transcript abundance correlates with malignancy grade in human astrocytomas. Int J Cancer. 2008;122:807-815.
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31.Fountoulakis M, Tsangaris GT, Maris A, Lubec G. The rat brain hippocampus proteome. J. Chromatogr. B. 2005;819:115-129.
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32.Peyrl A, Krapfenbauer K, Slavc I, Strobel T, Lubec G. Proteomic characterization of the human cortical neuronal cell line HCN-2. J Chem Neuroanat. 2003;26:171-8.
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34.Danielyan L, Schäfer R, Schulz A, Ladewig T, Lourhmati A, Buadze M, et al. Survival, neuron-like differentiation and functionality of mesenchymal stem cells in neurotoxic environment: the critical role of erythropoietin. Cell Death & Differentiation. 2009;16:1599-1614.
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36
ORIGINAL_ARTICLE
Inactivated Mycobacterium phlei inhalation ameliorates allergic asthma through modulating the balance of CD4+CD25+ regulatory T and Th17 cells in mice
Objective(s): Th2 response is related to the aetiology of asthma, but the underlying mechanism is unclear. To address this point, the effect of nebulized inhalation of inactivated Mycobacterium phlei on modulation of asthmatic airway inflammation was investigated. Materials and Methods: 24 male BALB/c mice were randomly divided into three groups: control group (Group A), asthma model group (Group B), and the medicated asthma model group (Group C). Group B and C were sensitized and challenged with ovalbumin (OVA). Group C was treated with aerosol M. phlei once daily before OVA challenge. Airway responsiveness in each group was assessed. All the animals were killed, and lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Inflammatory response, proportion of Th17 and CD4+CD25+ Treg cells, and the levels of cytokines were analyzed in lung tissue. Results: The proportion of Th17 cells and expression level of IL17, IL23, and IL23R were increased, while Foxp3 expression was decreased in Group B. Inhaling inactivated M. phlei inhibited airway inflammation and improved airway hyper-responsiveness, as well as peak expiratory flow (PEF). In addition, it significantly increased Th17 proportion, Foxp3 level, and the proportion of CD4+CD25+ Treg cells in lung tissue in Group C. Conclusion: Inactivated M. phlei was administered by atomization that suppressed airway inflammation and airway hyper responsiveness partially via modulating the balance of CD4+CD25+ regulatory T and Th17 cells.
https://ijbms.mums.ac.ir/article_7595_5ff61aa6f1448929c5e1be43223dab54.pdf
2016-09-01
953
959
10.22038/ijbms.2016.7595
Asthma
Atomization
Mycobacterium phlei
IL-17
Th17
Treg
Airway hyper-responsiveness
Moyu
Ming
:moyutiantian@163.com
1
Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China 530021
AUTHOR
Zhixi
Luo
zhixil173@163.com
2
Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China 530021
AUTHOR
Shengqiu
Lv
3
Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China 530021
AUTHOR
Qixiang
Sun
qxiang1981@163.com
4
Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China 530021
AUTHOR
Chaoqian
Li
hbb1983@126.com
5
Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China 530021
LEAD_AUTHOR
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ORIGINAL_ARTICLE
Protective effect of α-terpineol against impairment of hippocampal synaptic plasticity and spatial memory following transient cerebral ischemia in rats
Objective(s): Cerebral ischemia is often associated with cognitive impairment. Oxidative stress has a crucial role in the memory deficit following ischemia/reperfusion injury. α-Terpineol is a monoterpenoid with anti-inflammatory and antioxidant effects. This study was carried out to investigate the effect of α-terpineol against memory impairment following cerebral ischemia in rats. Materials and Methods: Cerebral ischemia was induced by transient bilateral common carotid artery occlusion in male Wistar rats. The rats were allocated to sham, ischemia, and α-terpineol-treated groups. α-Terpineol was given at doses of 50, 100, and 200 mg/kg, IP once daily for 7 days post ischemia. Morris water maze (MWM) test was used to assess spatial memory and in vivo extracellular recording of long-term potentiation (LTP) in the hippocampal dentate gyrus was carried out to evaluate synaptic plasticity. Malondialdehyde (MDA) was measured to assess the extent of lipid peroxidation in the hippocampus. Results: In MWM test, α-terpineol (100 mg/kg, IP) significantly decreased the escape latency during training trials (P<0.01). In addition, α-terpineol increased the number of crossings over the platform location and decreased average proximity to the target in probe trial (P<0.05). In electrophysiological recording, α-terpineol (100 mg/kg) facilitated the induction of LTP in the hippocampus which was persistent over 2 hr. α-Terpineol (100 and 200 mg/kg) also significantly lowered hippocampal MDA levels in rats subjected to cerebral ischemia. Conclusion: These findings indicate that α-terpineol improves cerebral ischemia-related memory impairment in rats through the facilitation of LTP and suppression of lipid peroxidation in the hippocampus.
https://ijbms.mums.ac.ir/article_7596_0f035d07b6956b8d9ac31097b86af8d2.pdf
2016-09-01
960
969
10.22038/ijbms.2016.7596
α-Terpineol
Cerebral ischemia
Long-term potentiation
Memory
Oxidative stress
Rats
Mahsa
Moghimi
mahsa.moghimi@sbmu.ac.ir
1
Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Siavash
Parvardeh
parvardehs@sbmu.ac.ir
2
Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Taraneh
Moini Zanjani
taraneh.m.zanjani@gmail.com
3
Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Shiva
Ghafghazi
ghafghazishiva@gmail.com
4
School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
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ORIGINAL_ARTICLE
The Expression implication of GDNF in ventral horn and associated remote cortex in rhesus monkeys with hemisected spinal cord injury
Objective(s): Glial cell line-derived neurotrophic factor (GDNF) can effectively promote axonal regeneration,limit axonal retraction,and produce a statistically significant improvement in motor recovery after spinal cord injury (SCI). However, the role in primate animals with SCI is not fully cognized. Materials and Methods:18 healthy juvenile rhesuses were divided randomly into six groups, observed during the periods of 24 hr, 7 days, 14 days, 1 month, 2 months, and 3 months after T11 hemisecting. The GDNF localization, changes in the injured region, and the remote associate cortex were detected by immunohistochemical staining. Results: Immunohistochemical staining showed that GDNF was located in the cytoplasm and the neurite of the neurons. Following SCI, the number of GDNF positive neurons in the ventral horn and the caudal part near the lesion area were apparently reduced at detected time points (P<0.05). Moreover, the number in the rostral part of the ventral horn in 7 day, 14 day, and 1 month groups were fewer than those in the caudal part. Importantly, in the contralateral cortex motor area, the positive neurons decreased sharply after hemi-SCI, while gradually increased and went back to normal in 3 months after hemi-SCI. Conclusion: To sum up, GDNF disruption in neurons occurred after SCI especially in cortex motor area. Intrinsic GDNF in the spinal cord, plays an essential role in neuroplasticity. Thereafter extrinsic GDNF supplementing may be a useful strategy to promote recovery after SCI.
https://ijbms.mums.ac.ir/article_7597_8de29ccbd91c93ca8613fea9f4fcceaa.pdf
2016-09-01
970
976
10.22038/ijbms.2016.7597
GDNF (glial cell line-derived neurotrophic factor)
Hemi-SCI (hemisection of spinal cord injury)
Macaca mulatta
Motor cortex
Spinal cord ventral horn
De-Lu
Qiu
1
Laboratory of Anesthesia and Critical Care Medicine, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, China
AUTHOR
Ting-Hua
Wang
nicolelulu@163.com
2
Laboratory of Anesthesia and Critical Care Medicine, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, China
LEAD_AUTHOR
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28
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29
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30
ORIGINAL_ARTICLE
Fluvoxamine inhibits some inflammatory genes expression in LPS/stimulated human endothelial cells, U937 macrophages, and carrageenan-induced paw edema in rat
Objective(s): Fluvoxamine is a well-known selective serotonin reuptake inhibitor (SSRI); Despite its anti-inflammatory effect, little is known about the precise mechanisms involved. In our previous work, we found that IP administration of fluvoxamine produced a noticeable anti-inflammatory effect in carrageenan-induced paw edema in rats. In this study, we aimed to evaluate the effect of fluvoxamine on the expression of some inflammatory genes like intercellular adhesion molecule (ICAM1), vascular cell adhesion molecule (VCAM1), cyclooxygenases2 (COX2), and inducible nitric oxide synthase (iNOS). Materials and Methods: An in vitro model of LPS stimulated human endothelial cells and U937 macrophages were used. Cells were pretreated with various concentrations of fluvoxamine, from 10-8 M to 10-6 M. For in vivo model, fluvoxamine was administered IP at doses of 25 and 50 mg/kg-1, before injection of carrageenan. At the end of experiment, the expression of mentioned genes were measured by quantitative real time (RT)-PCR in cells and in paw edema in rat. Results: The expression of ICAM1, VCAM1, COX2, and iNOS was significantly decreased by fluvoxamine in endothelial cells, macrophages, and in rat carrageenan-induced paw edema. Our finding also confirmed that IP injection of fluvoxamine inhibits carrageenan-induced inflammation in rat paw edema. Conclusion: The results of present study provide further evidence for the anti-inflammatory effect of fluvoxamine. This effect appears to be mediated by down regulation of inflammatory genes. Further studies are needed to evaluate the complex cellular and molecular mechanisms of immunomodulatory effect of fluvoxamine.
https://ijbms.mums.ac.ir/article_7598_f752ee25374daa4b6fd98297eff5e5db.pdf
2016-09-01
977
984
10.22038/ijbms.2016.7598
COX2
Fluvoxamine
Inflammation
ICAM1
INOS
VCAM1
Laleh
Rafiee
1
Applied Physiology Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Valiollah
Hajhashemi
hajhashemi@ pharm.mui.ac.ir
2
Department of Pharmacology and Toxicology, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Shaghayegh
Haghjooy Javanmard
shaghayegh.haghjoo@gmail.com
3
Applied Physiology Research Center, Isfahan Cardiovascular Research Institute and Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
1. Leonard BE. The immune system, depression and the action of antidepressants. ProgNeuropsycho-pharmacol Biol Psychiatry. 2001; 25:767–80.
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4. Sadeghi H, Hajhashemi V, Minaiyan M, Movahedian A, Talebi A. Further studies on anti-inflammatory activity of maprotiline in carrageenan-induced paw edema in rat. Int Immunopharmacol. 2013; 15:505–10.
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12. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods 2001; 25:402–8.
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34
ORIGINAL_ARTICLE
Immunomodulatory activities of gemifloxacin in mice
Objective(s):Gemifloxacin is a broad spectrum antibiotic and has shown excellent coverage against a wide variety of microorganisms. In this study, an attempt was made to evaluate the immunomodulatory potential of gemifloxacin in male swiss albino mice in vivo.
Materials and Methods: Three doses of gemifloxacin 25 mg/kg, 50 mg/kg and 75 mg/kg were used intraperitoneally (IP) for the evaluation of immune responses in mice. Delayed type hypersensitivity (DTH), heamagglutination assay, jerne hemolytic plaque formation assay and cyclophosphamide induced neutropenia assay were performed to evaluate the effect of gemifloxacin on immune responses.
Results: DTH assay has shown the significant immune suppressant potential of gemifloxacin at 25 mg/kg dose and 75mg/kg dose. Total leukocyte count (TLC) has shown decrease in leukocyte count (P<0.05) in drug treatment groups before cyclophosphamide administration and significant decrease (P<0.001) in leukocyte count after cyclophosphamide administration as compared to negative control group. Differential leukocyte count (DLC) has shown significant decrease (P<0.001) in percentage count of lymphocytes in 75 mg/kg treatment group in leukopenic mice while increase (P<0.01) in monocytes percentage in 50 mg/kg treatment group in leukopenic mice and increase in neutrophil percentage count (P<0.05) in all treatment groups was observed after cyclophosphamide administration. Humoral immune response is shown to be suppressed in dose dependent manner by both heamagglutination titre values (P<0.001) and jerne hemolytic plaque formation assay (P<0.001).
Conclusion: The results of this work clearly demonstrate that gemifloxacin has significant immunomodulatory potential.
https://ijbms.mums.ac.ir/article_7599_520d003f9030f5748d7645f6d011ac7e.pdf
2016-09-01
985
992
10.22038/ijbms.2016.7599
Gemifloxacin
Immunomodulatory
Immune response
Cell mediated
Humoral
Muhammad
Umair
pharmacistumairsargodhian@gmail.com
1
Department of Pharmacology and Toxicology, University of Veterinary and Animal Sciences, Lahore, Pakistan
AUTHOR
Aqeel
Javeed
aqeel.javeed@uvas.edu.pk
2
Department of Pharmacology and Toxicology, University of Veterinary and Animal Sciences, Lahore, Pakistan
LEAD_AUTHOR
Aamir
Ghafoor
aamir.ghafoor@uvas.edu.pk
3
University Diagnostics Laboratory, University of Veterinary and Animal Sciences, Lahore, Pakistan
AUTHOR
Muhammad
Ashraf
muhammad.ashraf@uvas.edu.pk
4
Department of Pharmacology and Toxicology, University of Veterinary and Animal Sciences, Lahore, Pakistan
AUTHOR
1. Wispelwey B, Schafer KR. Fluoroquinolones in the management of community-acquired pneumonia in primary care. Expert Rev Anti Infect Ther 2010; 8:1259-1271.
1
2. Albertson TE, Dean NS, El Solh AA, Gotfried MH, Kaplan C, Niederman MS. Fluoroquinolones in the management of community‐acquired pneumonia. Int J Clin Pract 2010; 64:378-388.
2
3. Bearden DT, Danziger LH. Mechanism of action of and resistance to quinolones. Pharmacotherapy 2001; 21:224S-232S.
3
4. Heaton VJ, Ambler JE, Fisher LM. Potent antipneumococcal activity of gemifloxacin is associated with dual targeting of gyrase and topoisomerase IV, an in vivo target preference for gyrase, and enhanced stabilization of cleavable complexes in vitro. Antimicrob Agents Chemother 2000; 44:3112-3117.
4
5. Yague G, Morris JE, Pan XS, Gould KA, Fisher LM. Cleavable-complex formation by wild-type and quinolone-resistant Streptococcus pneumoniae type II topoisomerases mediated by gemifloxacin and other fluoroquinolones. Antimicrob Agents Chemother 2002; 46:413-419.
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6. Saravolatz LD, Leggett J. Gatifloxacin, gemifloxacin, and moxifloxacin: the role of 3 newer fluoroquino-lones. Clin Infect Dis 2003; 37:1210-1215.
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7. Dalhoff A, Shalit I. Immunomodulatory effects of quinolones. Lancet Infect Dis 2003; 3:359-371.
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8. Araujo F, Slifer T, Li S, Kuver A, Fong L, Remington J. Gemifloxacin inhibits cytokine secretion by lipopolysaccharide stimulated human monocytes at the post‐transcriptional level. Clin Microbiol Infect 2004; 10:213-219.
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9. Dalhoff A. Immunomodulatory activities of fluoroquinolones. Infection 2005; 33:55-70.
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10. Sajid MS, Iqbal Z, Muhammad G, Sandhu MA, Khan MN, Saqib M, et al. Effect of ivermectin on the cellular and humoral immune responses of rabbits. Life Sci 2007; 80:1966-1970.
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12. Fulzele S, Satturwar P, Joshi S, Dorle A. Study of the immunomodulatory activity of Haridradi ghrita in rats. Indian J Pharmacol 2003; 35:51-54.
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13. Cho WCS, Leung KN. In vitro and in vivo immunomodulating and immunorestorative effects of Astragalus membranaceus. J Ethnopharmacol 2007; 113:132-141.
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14. Black CAP. Delayed type hypersensitivity: Current theories with a historic perspective. Dermatol Online J 1999; 5:7.
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18
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19
ORIGINAL_ARTICLE
Anti-inflammatory effect of Yu-Ping-Feng-San via TGF-β1 signaling suppression in rat model of COPD
Objective(s): Yu-Ping-Feng-San (YPFS) is a classical traditional Chinese medicine that is widely used for treatment of the diseases in respiratory systems, including chronic obstructive pulmonary disease (COPD) recognized as chronic inflammatory disease. However, the molecular mechanism remains unclear. Here we detected the factors involved in transforming growth factor beta 1 (TGF-β1)/Smad2 signaling pathway and inflammatory cytokines, to clarify whether YPFS could attenuate inflammatory response dependent on TGF-β1/Smad2 signaling in COPD rats or cigarette smoke extract (CSE)-treated human bronchial epithelial (Beas-2B) cells. Materials and Methods: The COPD rat model was established by exposure to cigarette smoke and intratracheal instillation of lipopolysaccharide, YPFS was administered to the animals. The efficacy of YPFS was evaluated by comparing the severity of pulmonary pathological damage, pro-inflammation cytokines, collagen related genes and the activation of TGF-β1/Smad2 signaling pathway. Furthermore, CSE-treated cells were employed to confirm whether the effect of YPFS was dependent on the TGF-β1/Smad2 signaling via knockdown Smad2 (Si-RNA), or pretreatment with the inhibitor of TGF-β1. Results: Administration of YPFS effectively alleviated injury of lung, suppressed releasing of pro-inflammatory cytokines and collagen deposition in COPD animals (P<0.05), whereas exogenous TGF-β1 promoted releasing of IL-1β, IL-6, TNFα (P<0.05). Administration YPFS reduced inflammatory response significantly, also down-regulated TGF-β1/Smad2 signaling in vivo and in vitro. Unexpectedly, knockdown Smad2 or inhibition of TGF-β1 abolished anti-inflammatory effect of YPFS in CSE-treated cells. Conclusion: YPFS accomplished anti-inflammatory effects mainly by suppressing phosphorylation of Smad2, TGF-β1/Smad2 signaling pathway was required for YPFS-mediated anti-inflammation in COPD rats or CSE-treated Beas-2B cells.
https://ijbms.mums.ac.ir/article_7600_7791deb9c5466e4ae548d10a9486e047.pdf
2016-09-01
993
1002
10.22038/ijbms.2016.7600
COPD
Pro-inflammatory
Cytokine
TGF-β1/Smad2
YPFS
Zhong-Shan
Yang
yangzhongshan@ynutcm.edu.cn
1
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
AUTHOR
Jin-Yuan
Yan
yanjinyuan1011@126.com
2
Central laboratory, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan
AUTHOR
Ni-Ping
Han
nini577@126.com
3
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
AUTHOR
Wei
Zhou
huadenga@yeah.net
4
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
AUTHOR
Yu
Cheng
cy811119@sina.com
5
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
AUTHOR
Xiao-Mei
Zhang
meimeizhang.net@163.com
6
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
AUTHOR
Ning
Li
1007556725@qq.com
7
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
AUTHOR
Jia-Li
Yuan
mutou1025@126.com
8
Faculty of Basic Medical Science, Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan
LEAD_AUTHOR
1.Hagstad S, Bjerg A, Ekerljung L, Backman H, Lindberg A, Rönmark E, et al. Passive smoking exposure is associated with increased risk of COPD in never smokers. Chest 2014; 145:1298-1304.
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10. Mohammad Hossein B, Leila GM. Lung inflammation changes and oxidative stress induced by cigarette smoke exposure in guinea pigs affected by Zataria multiflora and its constituent, carvacrol. BMC Complement Altern Med 2015;15:1-10.
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13. Wang B, Komers R, Carew R, Winbanks CE, Xu B, Herman-Edelstein M, et al. Suppression of microRNA-29 expression by TGF-β1 promotes collagen expression and renal fibrosis. J Am Soc Nephrol 2012; 23:252-265.
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24. Ma YT, Wang DH. Yu Ping Feng San stabilization treatment of chronic obstructive pulmonary disease pulmonary qi deficiency syndrome curative effect observation. Modern Traditional Chinese Med 2009:6-8.
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25. Wang CM, Jiang M, Wang HJ. Effect of NF-κB inhibitor on high‑mobility group protein B1 expression in a COPD rat model. Mol Med Rep 2013; 7:499-502.
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27. Du CY, Choi RC, Zheng KY, Dong TT, Lau DT, Tsim KW. Yu Ping Feng San, an ancient Chinese herbal decoction containing Astragali radix, Atractylodis macrocephalae Rhizoma and Saposhnikoviae radix, regulates the release of cytokines in murine macrophages. PLoS One 2013;8: e78622.
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38. Shen D, Xie X, Zhu Z, Yu X, Liu H, Wang H, et al. Screening active components from Yu-Ping-Feng-San for regulating initiative key factors in allergic sensitization. PLoS One 2014; 9:e107279.
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39. Du CYQ, Zheng KYZ, Bi CWC, Dong TTX, Lin HL, Tsim KWK. Yu Ping Feng San, an Ancient Chinese herbal decoction, Induces gene expression of anti-viral proteins and inhibits neuraminidase activity. Phytother Res 2015; 29:656-661.
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51. Sanchez-Muñoz F, Dominguez-Lopez A, Yamamoto-Furusho JK. Role of cytokines in inflammatory bowel disease. World J Gastroenterol 2008;14:4280-4288.
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53. Feizpour A, Mohammad Hossein B, Ghorbani A. Adipose-derived stromal cell therapy affects lung inflammation and tracheal responsiveness in guinea pig model of COPD. PLoS One 2014; 9:e108974.
53
54. Bonniaud P, Margetts PJ, Kolb M, Schroeder JA, Kapoun AM, Damm D, et al. Progressive transforming growth factor β1–induced lung fibrosis is blocked by an orally active ALK5 kinase inhibitor. Am J Respir Crit Care Med 2005;171:889-898.
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55. Rosendahl A, Checchin D, Fehniger TE, ten Dijke P, Heldin C-H, Sideras P. Activation of the TGF-β/activin-Smad2 pathway during allergic airway inflammation. Am J Respir Cell Mol Biol 2001; 25:60-68.
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56. Biernacka A, Dobaczewski M, Frangogiannis NG. TGF-β signaling in fibrosis. Growth factors. 2011; 29:196-202.
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57. Lan HY. Diverse roles of TGF-β/Smads in renal fibrosis and inflammation. Int J Biol Sci 2011; 7:1056-1067.
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58. Chung AC, Huang XR, Zhou L, Heuchel R, Lai KN, Lan HY. Disruption of the Smad7 gene promotes renal fibrosis and inflammation in unilateral ureteral obstruction (UUO) in mice. Nephrol Dial Transplant 2009; 24:1443-1454.
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59
ORIGINAL_ARTICLE
Potentiation of human papilloma vaccine candidate using naloxone/alum mixture as an adjuvant: increasing immunogenicity of HPV-16E7d vaccine
Objective(s): Many types of human papillomaviruses (HPVs) have been identified, with some leading to cancer and others to skin lesions such as anogenital warts. Studies have demonstrated an association between oncogenic HPV and cervical cancer and many researchers have focused on therapeutic vaccines development. At present, the modulatory effect of opioids on the innate and acquired immune system is characterized. Antagonists of opioid receptors such as naloxone (NLX) can contribute to the shifting Th2 response toward Th1. Herein; we studied the adjuvant activity of NLX/Alum mixture for improvement of the immunogenicity of HPV-16E7d vaccine.
Materials and Methods: The mice were administered different regimens of vaccine; E7d, E7d-NLX, E7d-Alum, E7d-NLX-Alum, NLX, alum and PBS via subcutaneous route for three times with two weeks interval. Two weeks after the last immunization, the sera were assessed for total antibody, IgG1 and IgG2a with an optimized ELISA method. The splenocytes culture supernatant was analyzed by ELISA for the presence of IL-4, IFN-g and IL-17 cytokines and lymphocyte proliferation was evaluated with Brdu method.
Results: Immunization of mice with HPV-16 E7d vaccine formulated in NLX/Alum mixture significantly increased lymphocyte proliferation and Th1 and Th17 cytokines responses compared to other experimental groups. Analysis of humoral immune responses revealed that administration of vaccine with NLX/Alum mixture significantly increased specific IgG responses and also isotypes compared to control groups.
Conclusion: NLX/Alum mixture as an adjuvant could improve cellular and humoral immune responses and the adjuvant maybe useful for HPV vaccines model for further studies in human clinical trial.
https://ijbms.mums.ac.ir/article_7601_7e0174fa36c71839d11391fe471bb02d.pdf
2016-09-01
1003
1009
10.22038/ijbms.2016.7601
Adjuvant
Alum
Naloxone
Papillomavirus
Vaccine
Mahsa
Yasaghi
marya4030@yahoo.com
1
Department of Basic Sciences, Faculty of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran (IAUPS)
AUTHOR
Mehdi
Mahdavi
mahdavivac@gmail.com
2
Department of Immunology, Pasteur Institute of Iran, Tehran, Iran
LEAD_AUTHOR
1. Burd EM. Human papillomavirus and cervical cancer. Clin Microbiol Rev 2003; 16:1-17.
1
2. Smith EM, Parker MA, Rubenstein LM, Haugen TH, Hamsikova E, Turek LP. Evidence for vertical transmission of HPV from mothers to infants. Infect Dis Obstet Gynecol 2010;2010: 326369.
2
3. Munger K, Baldwin A, Edwards KM, Hayakawa H, Nguyen CL, Owens M, et al. Mechanisms of human papillomavirus-induced oncogenesis. J Virol 2004; 78:11451-11460.
3
4. Avvakumov N, Torchia J, Mymryk JS. Interaction of the HPV E7 proteins with the pCAF acetyltransferase. Oncogene 2003; 22:3833-3841.
4
5. Fan R, Hou WJ, Zhao YJ, Liu SL, Qiu XS, Wang EH, et al. Overexpression of HPV16 E6/E7 mediated HIF-1alpha upregulation of GLUT1 expression in lung cancer cells. Tumour Biol 2015; 28:28.
5
6. Mora-Garcia ML, Monroy-Garcia A. [Immune response in cervical cancer. Strategies for the development of therapeutic vaccines]. Rev Med Inst Mex Seguro Soc 2015; 53:S206-211.
6
7. Giarre M, Caldeira S, Malanchi I, Ciccolini F, Leao MJ, Tommasino M. Induction of pRb degradation by the human papillomavirus type 16 E7 protein is essential to efficiently overcome p16INK4a-imposed G1 cell cycle Arrest. J Virol 2001; 75:4705-4712.
7
8. Lim YT. Vaccine adjuvant materials for cancer immunotherapy and control of infectious disease. Clin Exp Vaccine Res 2015; 4:54-58.
8
9. Coffman RL, Sher A, Seder RA. Vaccine adjuvants: putting innate immunity to work. Immunity 2010; 33:492-503.
9
10. Seubert A, Monaci E, Pizza M, O'Hagan DT, Wack A. The adjuvants aluminum hydroxide and MF59 induce monocyte and granulocyte chemoattractants and enhance monocyte differentiation toward dendritic cells. J Immunol 2008; 180:5402-5412.
10
11. Ninkovic J, Roy S. Role of the mu-opioid receptor in opioid modulation of immune function. Amino Acids 2013; 45:9-24.
11
12. Jamali A, Mahdavi M, Hassan ZM, Sabahi F, Farsani MJ, Bamdad T, et al. A novel adjuvant, the general opioid antagonist naloxone, elicits a robust cellular immune response for a DNA vaccine. Int Immunol 2009; 21:217-225.
12
13. Farahani SV, Aghasadeghi MR, Memarnejadian A, Faezi S, Shahosseini Z, Mahdavi M. Naloxone/Alum mixture, a potent adjuvant for HIV-1 vaccine: induction of cellular and poly-isotypic humoural immune responses. Pathog Glob Health 2015; 24.
13
14. Jamali A, Mahdavi M, Shahabi S, Hassan ZM, Sabahi F, Javan M, et al. Naloxone, an opioid receptor antagonist, enhances induction of protective immunity against HSV-1 infection in BALB/c mice. Microb Pathog 2007; 43:217-223.
14
15. Spellberg B, Edwards JE, Jr. Type 1/Type 2 immunity in infectious diseases. Clin Infect Dis 2001; 32:76-102.
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16. Marrack P, McKee AS, Munks MW. Towards an understanding of the adjuvant action of aluminium. Nat Rev Immunol 2009; 9:287-293.
16
17. Faezi S, Safarloo M, Amirmozafari N, Nikokar I, Siadat SD, Holder IA, et al. Protective efficacy of Pseudomonas aeruginosa type-A flagellin in the murine burn wound model of infection. Apmis 2014; 122:115-127.
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18. Katz CS. Humoral antibody formation in infants aged one to three months injected with a triple (diphtheria-tetanus-pertussis) alum-precipitated antigen, by William L. Bradford, MD, et al, Pediatrics, 1949;4:711-718. Pediatrics 1998; 102:207-209.
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19. Moon SH, Shin EC, Noh YW, Lim YT. Evaluation of hyaluronic acid-based combination adjuvant containing monophosphoryl lipid A and aluminum salt for hepatitis B vaccine. Vaccine 2015; 33:4762-4769.
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20. Morello CS, Kraynyak KA, Levinson MS, Chen Z, Lee KF, Spector DH. Inactivated HSV-2 in MPL/alum adjuvant provides nearly complete protection against genital infection and shedding following long term challenge and rechallenge. Vaccine 2012; 30:6541-6550.
20
21. Mahdavi M, Ebtekar M, Azadmanesh K, Khorramkhorshid HR, Rahbarizadeh F, Yazdi MH, et al. HIV-1 Gag p24-Nef fusion peptide induces cellular and humoral immune response in a mouse model. Acta Virol 2010; 54:131-136.
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22. Tomljenovic L, Shaw CA. Aluminum vaccine adjuvants: are they safe? Curr Med Chem 2011; 18:2630-2637.
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23. Mahdavi M, Ebtekar M, Khorram Khorshid HR, Azadmanesh K, Hartoonian C, Hassan ZM. ELISPOT analysis of a new CTL based DNA vaccine for HIV-1 using GM-CSF in DNA prime/peptide boost strategy: GM-CSF induced long-lived memory responses. Immunol Lett 2011; 140:14-20.
23
24. Jazani NH, Parsania S, Sohrabpour M, Mazloomi E, Karimzad M, Shahabi S. Naloxone and alum synergistically augment adjuvant activities of each other in a mouse vaccine model of Salmonella typhimurium infection. Immunobiology 2011; 216:744-751.
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25. Jazani NH, Sohrabpour M, Mazloomi E, Shahabi S. A novel adjuvant, a mixture of alum and the general opioid antagonist naloxone, elicits both humoral and cellular immune responses for heat-killed Salmonella typhimurium vaccine. FEMS Immunol Med Microbiol 2011; 61:54-62.
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29. Arezoo Shajiei ARM, Ghorbanali Shahabi, Ramin Farhoudi, Sobhan Faezi, Majid Tebianian, Nooshin Sohrabi, Mehdi Mahdavi. Pseudomonas aeruginosa Recombinant Flagellin Induced Poly-Isotypic Humoral Immune Responses in the Balb/C Mic. Jundishapur J Microbiol 2013; 6.
29
ORIGINAL_ARTICLE
Prednison provokes serum and vasoactive substances in a mice model of immune thrombocytopenia
Objective(s): The main objective of this study was to investigate the variations of β-endorphin (β-EP), vasoactive intestinal peptide (VIP), serotonin (5-HT) and norepinephrine (NE) of immune thrombocytopenia (ITP) mice as well as the regulatory mechanism of prednison.
Materials and Methods: Sixty BALB/c mice were randomly divided into control group, model group and prednison intervention group. ITP mice model was duplicated by injecting with glycoprotein-antiplatelet serum (GP-APS) except in control group. After ITP disease model was successful established, prednison was used in prednison intervention group. The β-EP, VIP, 5-HT and NE contents of ITP mice were detected by enzyme linked immunosorbent assay (ELISA).
Results:Compared with the values in control group, the detection values of VIP and 5-HT in model group declined, while the detection values of β-EP and NE increased. Compared with prednison intervention group, the detection values of VIP and 5-HT in model group increased, while the detection values of β-EP and NE showed no significant change.
Conclusion: In this study, the β-EP, VIP, 5-HT and NE contents in ITP mice injected with GP-APS were changed by prednison. It shows that prednison as the first-line therapy for ITP with effective hemostasis function is likely to increasing the contents of VIP and 5-HT. These results suggest the therapeutic value of prednison for the treatment of ITP.
https://ijbms.mums.ac.ir/article_7602_fbe8c0a4eab88ae50f406bf77aa7f249.pdf
2016-09-01
1010
1015
10.22038/ijbms.2016.7602
Immune thrombocytopenia
Mice
Norepinephrine VIP
β-EP
5-HT
Ling
Zhang
1
Dongzhimen Hosp. Beijing University of Chinese Medicine. No. 5 Haiyuncang, Dongcheng District, Beijing, China
AUTHOR
Ke
Chen
2
Dongzhimen Hosp. Beijing University of Chinese Medicine. No. 5 Haiyuncang, Dongcheng District, Beijing, China
AUTHOR
Tiantian
Li
bucmltt@126.com
3
Dongzhimen Hosp. Beijing University of Chinese Medicine. No. 5 Haiyuncang, Dongcheng District, Beijing, China
AUTHOR
Hao
He
tiantian_183@126.com
4
School of Pharmacy, Xi’an Medical College, Shanxi 710021, China
AUTHOR
Li
Hou
tiantian_183@163.com
5
Dongzhimen Hosp. Beijing University of Chinese Medicine. No. 5 Haiyuncang, Dongcheng District, Beijing, China
AUTHOR
Xiaoyong
Wu
bj.bucm@gmail.com
6
No. 1 Hospital Affiliated to Guiyang College of TCM, GuiYang 550001, China
AUTHOR
Yanping
Sun
419025578@qq.com
7
School of Pharmacy, Xi’an Medical College, Shanxi 710021, China
AUTHOR
Lei
Zheng
8
School of Pharmacy, Xi’an Medical College, Shanxi 710021, China
AUTHOR
Zhixiong
Chen
9
No. 1 Hospital Affiliated to Guangzhou University of Chinese Medicine, Guangzhou 510405, China
AUTHOR
Bei
Qin
18810702619@163.com
10
School of Pharmacy, Xi’an Medical College, Shanxi 710021, China
AUTHOR
Xinyi
Chen
chenxinyi0729@126.com
11
Dongzhimen Hosp. Beijing University of Chinese Medicine. No. 5 Haiyuncang, Dongcheng District, Beijing, China
AUTHOR
Shaodan
Tian
chenxinyi1954@126.com
12
Dongzhimen Hosp. Beijing University of Chinese Medicine. No. 5 Haiyuncang, Dongcheng District, Beijing, China
LEAD_AUTHOR
1. Singh A, Solanki A. High dose methylprednisolone: effective in pregnancy associated post-splenectomy refractory chronic immune thrombocytopenic purpura [J]. NJOG 2014; 2:64-66.
1
2. Pang MX, Huang XL, Li QY. Clinical observation of the combined applications of High-dose intravenous immunoglobulin and dexamethasone to treating idiopathic thrombocytopenic purpura of children. Acta Med Sinica 2012; 25:154-157.
2
3. Lang HY, Ma W, Zhang YY, SHI FQ, CHEN XY. Effect of long dan sheng xue granule on the peripheral hemogram, bone marrow megakaryocytes and serum PAIgG level in model mice with thrombocytopenic purpura. J Med Res 2014; 43:91-94.
3
4. Feng TT, Liu YB, Li ZY, et al. Production of monoclonal antibodies against enrofloxacin and the establishment of enzyme-linked immunosorbent assay. Isotopes, 2009; 22:5.
4
5. Provan D, Stasi R, Newland AC, Blanchette VS, Bolton-Maggs P, Bussel JB, et al. International consensus report on the investigation and management of primary immune thrombocytopenia. Blood 2010; 115:168-186.
5
6. Chen L, Liu XL. Relationship between β-endorphin and the therapeutic effect of opioids on the treatment of cancerous pain. Pain Clin J 2011; 7:63-66.
6
7. Zhu WL, Li JD, Zhang LF, Li H. Influence of moxibustion on content of β-endorphin in rats with adjuvant arthritis. J Beijing Univ Traditional Chinese Med 2011; 18:1-3.
7
8. Zhao WL, Zhao WS, Huang HW, Zhong LL. Effects of electroacupuncture on the hypothalamicβ-endorphin in rats with bone cancer pain. J Clin Acupuncture Moxibustion, 2013; 29:69-72.
8
9. Zang YS, Ji XL. Relationship between Anxiety and Serum β-endorphin in patients with Vitiligo. J Shanghai Jiaotong Univ 2012; 32:1347-1350.
9
10. Cheng H, Li RJ, Liang XL, et al. β-endorphin level expression in severe burn patients with depression in period of rehabilitation. J Med Theory Pract 2013; 26:985-990.
10
11. Huang C, Han LM. Electroacupuncture and immunity. Shandong Med J 2012; 52:91-92.
11
12. Cheng XW, Zheng QH, Li XL, et al. The research progress of pathogenic relationship between vasoactive intestinal peptide and some gastric motility disorders. Chin Gen Pract 2012; 15:237-240.
12
13. Jiang M, Liu DC. Vasoactive intestinal peptide and cardiovascular activity. Chongqing Med 2011; 40:1026-1028.
13
14. Ding F, Yang Z, Li G. Research progress of vasoactive intestinal peptide in COPD-related pulmonary hypertension. Int J Respir 2014; 34:1667-1670.
14
15. Gao RM, Lin X, Meng XY, Wang Q. Expression of motilin and vasoactive intestinal peptide in gastric mucosa of patients with primary bile reflux gastritis. World Chin J Digestol 2010; 18:722-725.
15
16. Zhou HY, Jiang HW, Wang MJ. Research progress of serotonin(5-HT) and its receptor. Shandong Med 2014; 54:90-93.
16
17. Chen M, Wang HF, Wang Y, Zhang XM. Meta-analysis of comparative efficacy between dopamine and norepinephrine in the treatment of septic shock. Shandong Med 2015; 55:52-54.
17
18. Liu C, Hu Z. Research progress of dopamine and norepinephrine for the treatment of septic shock. Med Recapitulate, 2011; 17:1361-1363.
18
ORIGINAL_ARTICLE
Total flavonoid extract from Coreopsis tinctoria Nutt. protects rats against myocardial ischemia/reperfusion injury
Objective(s): This study aimed to evaluate the protective effects of total flavonoid extract from Coreopsis tinctoria Nutt.(CTF)against myocardial ischemia/reperfusion injury (MIRI) using an isolated Langendorff rat heart model.
Materials and Methods: Left ventricular developed pressure (LVDP) and the maximum rate of rise and fall of LV pressure (±dp/dtmax) were recorded. Cardiac injury was assessed by analyzing lactate dehydrogenase (LDH) and creatine kinase (CK) released in the coronary effluent. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels were determined. Myocardial inflammation was assessed by monitoring tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), interleukin-8 (IL-8), and interleukin-6 (IL-6) levels. Myocardial infarct size was estimated. Cell morphology was assessed by 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin (HE) staining. Cardiomyocyte apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining.
Results: Pretreatment with CTF significantly increased the heart rate and increased LVDP, as well as SOD and GSH-Px levels. In addition, CTF pretreatment decreased the TUNEL-positive cell ratio, infarct size, and levels of CK, LDH, MDA, TNF-α, CRP, IL-6, and IL-8.
Conclusion: These results suggest that CTF exerts cardio-protective effects against MIRI via anti-oxidant, anti-inflammatory, and anti-apoptotic activities.
https://ijbms.mums.ac.ir/article_7603_9ed55b0331632a698718b216e42fdaf0.pdf
2016-09-01
1016
1023
10.22038/ijbms.2016.7603
Anti-apoptosis
Anti-oxidant
Anti-inflammatory
Cardio-protective
Coreopsis tinctoria Nutt
Ya
Zhang
zhangdaya0904@126.com
1
Ministry of Education, Pharmacy Shihezi University Xinjiang China
AUTHOR
Changsheng
Yuan
1007647886@qq.com
2
Ministry of Education, Pharmacy Shihezi University Xinjiang China
AUTHOR
He
Fang
358831940@qq.com
3
Ministry of Education, Pharmacy Shihezi University Xinjiang China
AUTHOR
Jia
Li
234945769@qq.com
4
Ministry of Education, Pharmacy Shihezi University Xinjiang China
AUTHOR
Shanshan
Su
245280242@qq.com
5
Ministry of Education, Pharmacy Shihezi University Xinjiang China
AUTHOR
Wen
Chen
chen-wen2000@126.com
6
Pharmacy Shihezi University Xinjiang China
LEAD_AUTHOR
1. Zweier JL, Talukder MA. The role of oxidants and free radicals in reperfusion injury. Cardiovasc Res 2006; 70:181-190.
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2. Pantos C, Bescond-Jacquet A, Tzeis S, Paizis I, Mourouzis I, Moraitis P, et al. Trimetazidine protects isolated rat hearts against ischemia-reperfusion injury in an experimental timing-dependent manner. Basic Res Cardiol2005; 100:154-160.
2
3. Najafi M. Effects of postconditioning, preconditioning and perfusion of L-carnitine during whole period of ischemia/ reperfusion on cardiac hemodynamic functions and myocardial infarction size in isolated rat heart. Iran J Basic Med Sci 2013; 16:648-655.
3
4. Hoffman JW Jr, Gilbert TB, Poston RS, Silldorff EP. Myocardial reperfusion injury: etiology, mechanisms, and therapies. J Extra Corpor Technol 2004; 36:391-411.
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5. Akhlaghi M, Bandy B. Mechanisms of flavonoid protection against myocardial ischemia-reperfusion injury. J Mol Cell Cardiol 2009; 46:309-317.
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6. Hodek P, Trefil P, Stiborova M. Flavonoids-potent and versatile biologically active compounds interacting with cytochromes P450. Chem Biol Interact 2002; 139:1-21.
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9. Babu PV, Liu D. Green tea catechins and cardiovascular health: an update. Curr Med Chem 2008; 15:1840-1850.
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10. Yu D, Li M, Tian Y, Liu J, Shang J. Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury. Life Sci2015; 122:15-25.
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11. Hirai M, Hotta Y, Ishikawa N, Wakida Y, Fukuzawa Y, Isobe F, et al.. Protective effects of EGCg or GCg, a green tea catechin epimer, against postischemic myocardial dysfunction in guinea-pig hearts. Life Sci2007; 80:1020-1032.
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12. Dias T, Bronze MR, Houghton PJ, Mota-Filipe H, Paulo A. The flavonoid-rich fraction of Coreopsis tinctoria promotes glucose tolerance regain through pancreatic function recovery in streptozotocin-induced glucose-intolerant rats. J Ethnopharmacol 2010; 132:483-490.
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13. Sun YH, Zhao J, Jin HT, Cao Y, Ming T, Zhang LL, et al. Vasorelaxant effects of the extracts and some flavonoids from the buds of Coreopsis tinctoria. Pharm Biol 2013; 51:1158-1164.
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14. Yao L, Li L, Li X, Li H, Zhang Y, Zhang R, et al. The anti-inflammatory and antifibrotic effects of Coreopsis tinctoria Nutt on high-glucose-fat diet and streptozotocin-induced diabetic renal damage in rats. BMC Complement Alternat Med 2015; 15:314.
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15. Lan S, Lin J, Zheng N. Evaluation of the antioxidant activity of Coreopsis tinctoria Nuff. and optimisation of isolation by response surface methodology. Acta Pharm 2014; 64:369-378.
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16. Guo LM, Zhang WS, Li SM, Ho CT. Chemical and nutraceutical properties of Coreopsis tinctoria. J Funct Foods 2015; 13:11-20.
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18. Zhao P, Qi C, Wang G, Dai XP, Hou XH. Enrichment and purification of total flavonoids from Cortex Juglandis Mandshuricae extracts and their suppressive effect on carbon tetrachloride-induced hepatic injury in Mice. J Chromatogr B 2015; 1007:8-17.
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20. Badavi M, Sadeghi N, Dianat M, Samarbafzadeh A. Effects of gallic Acid and cyclosporine a on antioxidant capacity and cardiac markers of rat isolated heart after ischemia/reperfusion. Iran Red Crescent Med J 2014; 16:e16424.
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24. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol 2003; 285:H579-588.
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ORIGINAL_ARTICLE
Effects of Lycium barbarum. polysaccharide on type 2 diabetes mellitus rats by regulating biological rhythms
Objective(s): Type 2 diabetes mellitus (T2DM) is associated with circadian disruption. Our previous experimental results have showed that dietary Lycium barbarum. polysaccharide (LBP-4a) exhibited hypoglycemic and improving insulin resistance (IR) activities. This study was to explore the mechanisms of LBP-4a for improving hyperglycemia and IR by regulating biological rhythms in T2DM rats.
Materials and Methods:The rats of T2DM were prepared by the high-sucrose-fat diets and injection of streptozotocin (STZ). The levels of insulin, leptin and melatonin were measured by enzyme linked immunosorbent assay (ELISA). The effect of LBP-4a on mRNA expression of melatonin receptors (MT2) in epididymal adipose tissue was evaluated by RT-PCR. The expression of CLOCK and BMAL1 in pancreatic islet cells was detected by Western blotting.
Results: Our data indicated that the 24-hr rhythm of blood glucose appeared to have consistent with normal rats after gavaged administration of LBP-4a for each day of the 4 weeks, and the effects of hypoglycemia and improving hyperinsulinemia in T2DM rats treated at high dose were much better than that at low dose. The mechanisms were related to increasing MT2 level in epididymal adipose tissue and affecting circadian clocks gene expression of CLOCK and BMAL1 in pancreatic islet cells.
Conclusion: LBP-4a administration could treat T2DM rats. These observations provided the background for the further development of LBP-4a as a potential dietary therapeutic agent in the treatment of T2DM.
https://ijbms.mums.ac.ir/article_7604_8a70bcde18e8baad5d5f8be94ed417f7.pdf
2016-09-01
1024
1030
10.22038/ijbms.2016.7604
Circadian clocks
Lycium barbarum
Melatonin receptors
Polysaccharide
Type 2 diabetes mellitus
Rui
Zhao
zr601@163.com
1
Department of Pharmaceutical Engineering, College of Life Science & Biotechnology, Heilongjiang August First Land Reclamation University, Daqing High-Tech Industrial Development Zone, China
AUTHOR
Xu
Gao
zhaoruier@sina.com
2
Department of Biochemistry and Molecular Biology, Basic Medical Science College, Harbin Medical University, Harbin China
LEAD_AUTHOR
Tao
Zhang
zht13946447995@126.com
3
School of Basic Medical Sciences, Jiamusi University, No.188 Xuefu Street, Jiamusi City, Heilongjiang Province, China
AUTHOR
Xing
Li
4
Department of Nephrology, Daqing people’s Hospital, No.213 Jianshe Road, Gaoxin District, Daqing City, Heilongjiang Province, China
AUTHOR
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