ORIGINAL_ARTICLE
Nonsense-mediated mRNA decay among coagulation factor genes
Objective(s): Haemostasis prevents blood loss following vascular injury. It depends on the unique concert of events involving platelets and specific blood proteins, known as coagulation factors. The clotting system requires precise regulation and coordinated reactions to maintain the integrity of the vasculature. Clotting insufficiency mostly occurs due to genetically inherited coagulation factor deficiencies such as hemophilia. Materials and Methods: A relevant literature search of PubMed was performed using the keywords coagulation factors, Nonsense-mediated mRNA decay and premature translation termination codons. Search limitations included English language and human-based studies. Results: Mutations that cause premature translation termination codons probably account for one-third of genetically inherited diseases. Transcripts bearing aberrant termination codons are selectively identified and eliminated by an evolutionarily conserved posttranscriptional pathway known as nonsense-mediated mRNA decay (NMD). There are many pieces of evidence of decay among coagulation factor genes. However, the hemophilia gene (F8) does not seem to be subjected to NMD. Since the F8 gene is located on the X-chromosome, a connection between X-linked traits and mRNA decay could be assumed. Conclusion: Considering that not all genes go through decay, this review focuses on the basics of the mechanism in coagulation genes. It is interesting to determine whether this translation-coupled surveillance system represents a general rule for the genes encoding components of the same physiological cascade.
https://ijbms.mums.ac.ir/article_6804_a90d929cf0e0d12422231471e851603c.pdf
2016-04-01
344
349
10.22038/ijbms.2016.6804
Coagulation factors
Nonsense-mediated mRNA- decay
Premature translation -termination codons
Shirin
Shahbazi
sh.shahbazi@modares.ac.ir
1
Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
LEAD_AUTHOR
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ORIGINAL_ARTICLE
Tracheal overexpression of IL-1β, IRAK-1 and TRAF-6 mRNA in obese-asthmatic male Wistar rats
Objective(s): Human and animal studies have shown a close relationship between obesity and asthma severity. Here, we examined the effects of diet-induced obesity (DIO) on the expression levels of IL-1β, IRAK-1 and TRAF-6 mRNA in male Wistar rats tracheal after sensitization with ovalbumin (OVA).
Materials and Methods:Twenty male Wistar rats divided to four groups, included, control group with normal diet (C+ND), OVA-sensitized group with normal diet (S+ND), control group with high-fat diet (C+HFD), and OVA-sensitized group with high-fat diet (S+HFD). All animals fed for 8 weeks with standard pelts or high-fat diet, and then were sensitized and challenged with OVA or saline for another 4 weeks with designed regimens. At the end of study, trachea isolated and examined for expression levels of IL-1β, IRAK-1 and TRAF-6 mRNA with RT-PCR method.
Results:Diet-induced obesity groups developed increased weight, obesity indexes and lipid profiles (P<0.05 to P<0.001). The expression levels of IL-1β mRNA in OVA-sensitization groups (S+ND and S+HFD) showed a significantly increased when compared with control group. Also in S+HFD group, expression level of TRAF-6 mRNA was higher than other groups (P<0.001). IRAK-1 expression level was high in S+HFD compared with control group.IL-1β and TRAF-6 mRNA correlated positively with obesity indexes.
Conclusion:The results showed that DIO causes overexpression of IL-1β, IRAK-1 and TRAF-6 mRNA in an experimental model of asthma. Our results suggested that in obese-asthmatic conditions locally production and activation of pro-inflammatory agents can be increased. These findings showed that possible mechanism for obesity-asthma relationships.
https://ijbms.mums.ac.ir/article_6805_fce5856c822976fd81c3da30a8d33580.pdf
2016-04-01
350
357
10.22038/ijbms.2016.6805
Asthma
IL-1β
IRAK-1
Obesity
Tracheal
TRAF-6
Mohammad Reza
Aslani
mr_aslani@hotmail.com
1
Tuberculosis and Lung Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Rana
Keyhanmanesh
2
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Amir Mehdi
Khamaneh
khamanehamir@gmail.com
3
School of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Mehran Mesgari
Abbasi
4
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Maryam
Fallahi
m.fallahi@gmail.com
5
Department of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Mohammad Reza
Alipour
alipourmr52@yahoo.com
6
Tuberculosis and Lung Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1.Beuther DA, Sutherland ER. Overweight, obesity, and incident asthma: a meta-analysis of prospective epidemiologic studies. Am J Respir Crit Care Med 2007;175:661-666.
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40
ORIGINAL_ARTICLE
Apoptosis inducing capacity of Holothuria arenicola in CT26 colon carcinoma cells in vitro and in vivo
Objective(s):Sea cucumber is one of the classes of echinoderms, which is considered as a health marine product and possess various biological characteristics with therapeutic application. The present investigation attempted to evaluate the potential of anti-cancer Persian Gulf sea cucumber species Holothuria arenicola (H. arenicola) aqueous extract on mice colon carcinoma cells in vitro and in vivo.
Materials and Methods: The CT26 carcinoma cells were treated with various concentrations of extract in 24 and 48 hr, and then its anti-proliferative effect was measured by MTT assay and morphological observations. The apoptotic effect was examined by fluorescence microscopy (DNA fragmentation assay), Flow cytometry, caspase-3 and -9 colorimetric assays. The in vivo anti-tumor efficacy of sea cucumber extract on CT26 tumor cells transplanted in BALB/c mice was also investigated.
Results: The results showed that the water extract of sea cucumber revealed remarkable anti-proliferative effect on CT26 tumor cells with IC50= 31 µg/ml with recruitment of intrinsic apoptotic pathway in vitro. In addition, the colon tumor volume in treated groups remarkably reduced in homozygous mice. Histopathological examination elucidated that sea cucumber extract attenuated tumor size and volume along with apoptosis characteristics. Moreover, RT-PCR analysis revealed that sea cucumber extract induced intrinsic apoptosis in vivo through suppression of Bcl-2 expression.
Conclusion: Our data confirmed this notion that sea cucumber administrates anti-cancer effect that can be used as complementary in preclinical experiments, so further characterization are recommended for detection sea cucumber metabolites and clinical application.
https://ijbms.mums.ac.ir/article_6806_e2e48be08d816205e87406031b9b4577.pdf
2016-04-01
358
365
10.22038/ijbms.2016.6806
Apoptosis
Anti-tumor effect
Colon cancer
Marine
Sea cucumber
Javad
Baharara
bahararaj@yahoo.com
1
Department of Biology, Research Center for Applied Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Elaheh
Amini
aminie@mus.ac.ir
2
Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran
AUTHOR
Mahbubeh
Afzali
mahbubeh50@yahoo.com
3
MSc Student of Developmental Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Najme
Nikdel
4
MSc Student of Developmental Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Asma
Mostafapour
asma.mostafapour12@gmail.com
5
MSc Student of Developmental Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran
AUTHOR
Mohammad Amin
Kerachian
kerachianma@mums.ac.ir
6
Medical Genetics Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1.Aliabadi A, Eghbalian E, Kiani A. Synthesis and evaluation of the cytotoxicity of a series of 1,3,4-Thiadiazole based compounds as anticancer agents. Iran J Basic Med Sci 2013; 16:1133-1138.
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2.Murthy KNC, Jayaprakasha GK, Patil BS. The natural alkaloid berberine targets multiple pathways to induce cell death in cultured human colon cancer cells. Eur J Pharmacol 2012; 688:14–21.
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3
4.Varshosaz J, Hassanzadeh F, Sadeghi-aliabadi H, Firozian F. Uptake of Etoposide in CT-26 cells of colorectal cancer using folate targeted dextran stearate polymeric micelles. Biomed Res Int 2014; 2014:1–11.
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5. Zhou R, Huang WJ, Ma C, Zhou Y, Yao YQ, Wang YX, et al. HOCl oxidation-modified CT26 cell vaccine inhibits colon tumor growth in a mouse model. Asian Pacific J Cancer Prev 2012; 13:4037–4043.
5
6. Deng Sh, Hu B, An HM, Du Q, Xu L, Shen K, et al. Teng-Long-Bu-Zhong-Tang, a Chinese herbal formula, enhances anticancer effects of 5 - Fluorouracil in CT26 colon carcinoma. BMC Complement Altern Med 2013; 13:1-11.
6
7.Momtazi-borojeni A, Behbahani M, Sadeghi Aliabadi H. Antiproliferative activity and apoptosis induction of crude extract and fractions of Avicennia marina. Iran J Basic Med Sci 2013; 16:1203-1208.
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9. Anter J, Fernández-bedmar Z, Villatoro-pulido M, Demyda-peyras S, Moreno-millán M, Alonso-moraga Á, et al. A pilot study on the DNA-protective, cytotoxic, and apoptosis-inducing properties of olive-leaf extracts. Mutat Res 2011; 723:165-170.
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11. Thangam R, Sathuvan M, Poongodi A, Suresh V, Pazhanichamy K, Sivasubramanian S, Kanipandian N, et al. Activation of intrinsic apoptotic signaling pathway in cancer cells by Cymbopogon citratus polysaccharide fractions. Carbohydr Polym 2014; 107:138-150.
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12. Xia Y, Liu Z, Li Z. Effects of high hydrostatic pressure treatment on physicochemical characteristics of Sea cucumber. J Food Sci Eng 2012; 2:227–238.
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13. Soltani M, Parivar K, Baharara J, Kerachian MA, Asili j. Putative mechanism for apoptosis-inducing properties of crude saponin isolated from sea cucumber (Holothurialeucospilota) as an antioxidant compound. Iran J Basic Med Sci 2015; 18:180-187.
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35
ORIGINAL_ARTICLE
Parental cigarette smoking, transforming growth factor-alpha gene variant and the risk of orofacial cleft in Iranian infants
Objective(s):We investigated the influence of genetic variation of the transforming growth-factor alpha (TGFA) locus on the relationship between smoking and oral clefts. Materials and methods:In this study 105 Iranian infants with non-syndromic cleft lip/palate and 218 controls with non-cleft birth defects were examined to test for associations among maternal exposures, genetic markers, and oral clefts. Maternal and parental smoking histories during pregnancy were obtained through questionnaire. DNA was extracted from newborn screening blood samples, and genotyping of the BamHI polymorphism in the TGFA gene was performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. A number of factors including gender of the newborns, type of oral cleft, consanguinity of the parents, as well as the mother’s age and education were evaluated as potential confounders and effect modifiers. Results: Maternal smoking, in the absence of paternal smoking, was associated with an increased risk for CL/P (OR = 19.2, 95% CI = [(6.2-59.5)]) and cleft palate only (OR =48.7, 95% CI = [(8-29.3)]). If both parents smoked, risks were generally greater (OR = 55.6, 95% CI = [12-20.25]). Analyses for the risk of clefting from maternal smoking, stratified by the presence or absence of the TGFA/BamH1variant, revealed that the risk of clefting among the infants with the TGFA/BamH1 variant when their mothers smoked cigarettes was much greater than the infants who had non-smoker mothers (P=0.001, OR=10.4,95% CI=[3.2,33.6]). Conclusion:The results of this study indicate that first-trimester maternal smoking and infant TGFA locus mutations are both associated with nonsyndromic cleft lip and/or palate (CL/P).
https://ijbms.mums.ac.ir/article_6807_00980a84018a1d090ec5b14cfa975193.pdf
2016-04-01
366
373
10.22038/ijbms.2016.6807
Cleft Lip/Palate
Polymorphism
Smoking
Transforming growth-
factor alpha
Asghar
Ebadifar
a.ebadifar@sbmu.ac.ir
1
Dentofacial Deformities Research Center, Research Institute of Dental Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Roya
Hamedi
2
Dental Carries Prevention Research Center, Qazvin University of Medical Sciences, Qazvin, Iran
AUTHOR
Hamid Reza
KhorramKhorshid
3
Genetic Research Centre, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
AUTHOR
Koorosh
Kamali
4
Department of Public Health, School of Public Health, Zanjan University of Medical Sciences, Zanjan, Iran
AUTHOR
Fatemeh Aghakhani
Moghadam
5
Bachelors of Medical Laboratory Sciences, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
AUTHOR
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59
ORIGINAL_ARTICLE
Effects of 1,25-dihydroxyvitamin D3 on IL-17/IL-23 axis, IFN-γ and IL-4 expression in systemic lupus erythematosus induced mice model
Objective(s): Systemic lupus erythematosus (SLE) is a multi-factorial autoimmune disease which may be characterized by T lymphocytes dysfunctions. Th17 cells have been identified as new effector cells, which play an important role in the pathogenesis. In recent years, immunomodulatory effect of vitamin D3 has been noticed. In the present experiment, the effect of vitamin D3 on the expression of IL-17, IL-23, IL-4 and IFN-γ were assessed in activated chromatin-induced mouse model for SLE. Materials and Methods: Five groups of mice were included in this study; Group one received active chromatin +CFA + PBS; Group 2 received vitamin D3 starting 2 weeks before disease induction; Group 3 received vitamin D3 (50 ng/day) starting with the disease establishment; Group 4 received non active chromatin +CFA + PBS; Group 5 received CFA + PBS. On day 56 splenocytes were isolated and gene expression of interleukin IL-17, IL-23, IL-4 and IFN-γ were analyzed by Real-Time PCR method. Proteinuria and serum anti-dsDNA and Th17 levels were measured using commercial kits. Results: The results showed that IL-17, IL-23, and IFN-γ mRNA expression, and IL-17 titers were decreased remarkably and that of IL-4 increased in mice which received vitamin D3 before SLE induction. Administration of vitamin D3 after the establishment of SLE failed to affect the IL-17 or IL-23 mRNA levels. Lastly, pre-treatment of mice with vitamin D3 decreased the anti-ds DNA antibody titer. Conclusion: Our findings showed that vitamin D3 supplementation in lupus induced mice through modulating the expression rate of some inflammatory cytokines diminished the inflammatory conditions in SLE.
https://ijbms.mums.ac.ir/article_6808_c38a50abb73423fd4055a62e5ab1f19d.pdf
2016-04-01
374
380
10.22038/ijbms.2016.6808
Cytokines
Mice
Systemic lupus-erythematosus
Th17 cells
Vitamin D
Fatemeh
Faraji
farajif901@mums.ac.ir
1
Immunology Research Center, BuAli Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Maryam
Rastin
maryam_rastin1987@yahoo.com
2
Immunology Research Center, BuAli Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fahimeh
Lavi Arab
lavif931@mums.ac.ir
3
Immunology Research Center, BuAli Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahmoudreza
Kalantari
4
Pathology Department, Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Shahrzad Zamani
Taghizadeh Rabe
5
Immunology Research Center, BuAli Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Nafise
Tabasi
6
Immunology Research Center, BuAli Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahmoud
Mahmoudi
said.aslany@gmail.com
7
Immunology Research Center, BuAli Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Tsokos GD. Systemic lupus erythematosus. New Engl J Med 2011; 365: 2110-2121.
1
2. D. P. D’Cruz, M. A. Khamashta, and G. R. Hughes, “Systemic lupus erythematosus. Lancet 2007; 369: 587– 596.
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3. Lewis JE, Fu SM, Gaskin F. Autoimmunity, end organ damage, and the origin of autoantibodies and autoreactive T cells in systemic lupus erythematosus. Discov Med 2013; 15: 85-92.
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5. Qiao B, Wu J, Chu YW, Wang Y, Wang DP, Wu HS et al. Induction of systemic lupus erythematosus-like syndrome in syngeneic mice by immunization with activated lymphocyte-derived DNA. Rheumatology (Oxford) 2005; 44:1108-1114.
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6. Shah K, Lee WW, Lee SH, Kim SH, Kang SW, Craft J et al. Dysregulated balance of TH17 and TH1 cells in systemic lupus erythematosus. Arthritis Res Ther 2010; 12: R53.
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14. Cutolo M. Further emergent evidence for the vitamin D endocrine system involvement in autoimmune rheumatic disease risk and prognosis. Ann Rheum Dis 2013; 72: 473-475.
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15. Szodoray P, Nakken B, Gaal J, Jonsson R, Szegedi A, Zold E, et al. Complex role of vitamin D in autoimmune diseases. Scand J Immunol 2008; 68: 261-269.
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16. Chang SH, Chung Y, Dong C. Vitamin D suppresses TH17 cytokine production by inducing C/EBP homologous protein (CHOP) expression. J Biol Chem 2010; 285: 38751-38755.
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17. Wen ZK, Xu W, Xu L, Cao OH, Wang Y, Chu YW, et al. DNA hypomethylation is crucial for apoptotic DNA to induce systemic lupus erythematosus-like autoimmune disease in SLE-nonsusceptible mice. Rheumatology 2007; 46: 1796-1803.
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18. Apostolidis SA, Lieberman LA, Kis-Toth K, Crispin JC, Tsokos GC. The dysregulation of cytokine networks in systemic lupus erythematosus. J Interferon Cytokine Res 2011; 31: 769-779.
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19. Ding-Lei Su ZM, Min-Ning S, Xia L, Ling-Yun S. Roles of pro- and anti-inflammatory cytokines in the pathogenesis of SLE. J Biomed Biotech 2012; 2012: 347141.
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20. Edgerton C, Crispín JC, Moratz CM, Betteli E, Oukka M, Simovic M, et al. IL-17 producing CD4+ T-cells mediate accelerated ischemia/reperfusion-induced injury in autoimmunity-prone mice. Clin Immunol 2009; 130: 313-321.
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21. Zhang Z, Kyttaris VC, Tsokos GC. The role of IL-23/IL-17 axis in lupus nephritis. J Immunol 2009; 183: 3160-3169.
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22. Kyttaris VC, Zhang Z, Kuchroo VK, Oukka M, Tsokos GC. Cutting Edge: IL-23 receptor deficiency orevents development of lupus nephritis in C57BL/6–lpr/lpr mice. J Immunol 2010; 184: 4605-4609.
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23. Tabasi N, Rastin M, Mahmoudi M, Ghoryani M, Mirfeizi Z, Zamani SH, et al. Influence of Vitamin D on cell cycle, apoptosis, and some apoptosis related molecules in systemic lupus erythematosus. Iran J Basic Med Sci 2015; 18: 1107-1111.
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24. Lavi Arab F, Rastin M, Faraji F, Zamani Taghizadeh Rabe S, Tabasi N, Khazaee M, et al. Assessment of 1,25-D3 effects on Treg cells and their related molecules in active chromatin lupus induced Balb/c mice. Immunopharmacol Immunotoxicol 2015; 37: 12-18.
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25. Wahono CS, Rusmini H, Soelistyoningsih D, Hakim R, Handono K, Endharti AT, et al. Effects of 1,25(OH)2D3 in immune response regulation of systemic lupus erithematosus (SLE) patient with hypovitamin D. Int J Clin Exp Med 2014; 7: 22-31.
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27. Deluca HF, Cantorna MT. Vitamin D: Its role and uses in immunology. FASEB J 2001; 15: 2579-2585.
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28. Koizumi T, Nakao Y, Matsui T, Nakagawa T, Matsuda S, Komoriya K, et al. Effects of corticosteroid and 1,24R-dihydroxy-vitamin D3 administration on lymphoproliferation and autoimmune disease in MRL/MP-lpr/lpr mice. Int Arch Allergy Appl Immunol 1985; 77: 396-404.
28
29. Vaisberg MW, Kaneno R, Franco MF, Mendes NF. Influence of cholecalci-ferol (vitamin D3) on course of experimental systemic lupus erythematosus in F1 (NZB x W) mice. J Clin Lab Anal 2000; 14: 91-96.
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30. Reihani H, Rastin M, Mahmoudi M, Ghoryani M, Abdlahi N, Tabasi N, et al. Influence of 1 Alpha, 25-Dihydroxyvitamin D3 on T Helper 17 Cells and Related Cytokines in Systemic Lupus
30
Erythematosus, Iran J Immunol 2015; 12: 82-93.
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31. Onishi RM, Gaffen SL. Interleukin-17 and its target genes: mechanisms of interleukin-17 function in disease. Immunology 2010; 129:311–321.
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32. Langrish CL, Chen Y, Blumenschein WM, Mattson J, Basham B, Sedgwick JD, et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med 2005; 201:233–240
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33. Raza A, Yousaf W, Giannella R, Shata M. Th17 cells: interactions with predisposing factors in the immunopathogenesis of inflammatory bowel disease. Expert Rev Clin Immunol 2012; 8: 161–168.
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34. Daniel C, Sartory NA, Zahn N, Radeke HH, Stein JM. Immune modulatory treatment of trinitrobenzene sulfonic acid colitis with calcitriol is associated with a change of a T-helper (TH) 1/TH17 to a TH2 and regulatory T-cell profile. J Pharmacol Exp Ther 2008; 324: 23-33.
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35. Ding-Lei Su ZM, Min-Ning S, Xia L, Ling-Yun S. Roles of pro- and anti-inflammatory cytokines in the pathogenesis of SLE. J Biomed Biotech 2012; 2012: 347141.
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36. Jeffery LE, Burke F, Mura M, Zheng Y, Qureshi OS, Hewison M, et al. 1,25 Dihydroxyvitamin D3 and IL-2 combine to inhibit T Cell production of inflammatory cytokines and promote development of regulatory T Cells expressing CTLA-4 and Foxp3. J Immunol 2009; 183: 5458-5467.
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37. Terrier B, Derian N, Schoindre Y, Charra W, Geri G, Zahr N, et al. Restoration of regulatory and effector T cell balance and B cell homeostasis in systemic lupus erythematosus patients through vitamin D supplementation. Arthritis Res Therap 2012; 14: R22.
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38. Singh A, Kamen DL. Potential benefits of vitamin D for patients with systemic lupus erythematosus. Dermatoendocrinol 2012; 4: 146-51.
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39. Ghoryani M, Sahebari M, Mahmoudi M, Abdollahi N, Reihani H, Zamani SH, et al. Immunomodulatory Vitamin D effects on regulatory T-cells and cytokines in an in vitro study on patients with systemic lupus erythematosus. Food and Agricultural Immunology 2016; 27: 377-387.
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41. Dean GS, Anand A, Blofeld A, Isenberg DA, Lydyard PM. Characterization of CD3+CD4-CD8- (double negative) T-cells in patients with systemic lupus erythematosus: Production of IL-4. Lupus 2002; 11: 501-507.
42
ORIGINAL_ARTICLE
Expression of the Mir-133 and Bcl-2 could be affected by swimming training in the heart of ovariectomized rats
Objective(s): The beneficial and more potent role of exercise to prevent heart apoptosis in ovariectomized rats has been known. The aim of this study was to examine the effects of swimming training on cardiac expression of Bcl-2, and Mir-133 levels and glycogen changes in the myocyte.
Materials and Methods: Forty animals were separated into four groups as control, sham, ovariectomy (OVX) and ovariectomized group with 8 weeks swimming training (OVX.E). Training effects were evaluated by measuring lipid profiles, Bcl-2 and Mir-133 expression levels in the cardiac tissue. Grafts were analyzed by reverse transcription–polymerase chain reaction for Bcl-2 mRNA and Mir-133 and by Western blot for Bcl-2 protein.
Results: Ovariectomy down-regulated Bcl-2 and Mir-133 expression levels in the cardiac tissue, and swimming training up-regulated their expression significantly (P<0.05).
Conclusion: Our results showed that regular exercise as a physical replacement therapy could prevent and improve the effects of estrogen deficiency in the cardia.
https://ijbms.mums.ac.ir/article_6809_463b75af1b792a62a9a4ec9ad0292070.pdf
2016-04-01
381
387
10.22038/ijbms.2016.6809
Bcl-2
Heart
Mir-133
Ovariectomy
Swimming training
Parisa
Habibi
dr.habibi2007@yahoo.com
1
Department of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Alireza
Alihemmati
hemmati@yahoo.com
2
Department of Histology & Embryology, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Alireza
NourAzar
3
Department of Physiology, Tabriz Branch, Islamic Azad University, Tabriz, Iran
AUTHOR
Hadi
Yousefi
4
Department of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Safieh
Mortazavi
mortazavi.59152@gmail.com
5
Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Nasser
Ahmadiasl
n.ahmadiacl@gmail.com
6
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1. Shuster LT, Rhodes DJ, Gostout BS, Grossardt BR, Rocca WA. Premature menopause or early menopause: long-term health consequences. Maturitas 2010; 65:161-166.
1
2. Mahdavian M, Abbassian H. Major cardiovascular risk factors for menopausal and non-menopausal women compared with men of the same age in Mashhad, Iran. J Midwifery Reprod Health 2014; 2:136-142.
2
3. Kim JK, Levin ER. Estrogen signaling in the cardiovascular system. Nucl Recept Signal 2006; 4: e013.
3
4. Hsu CC, Ou HC, Lee SD. Effects of exercise training on cardiac mitochondrial apoptosis in ovariectomized rats. FASEB J 2010; 24:601-605.
4
5. Liou CM, Yang AL, Kuo CH, Tin H, Huang CY, Lee SD. Effects of 17beta‐estradiol on cardiac apoptosis in ovariectomized rats. Cell Biochem Funct 2010; 28:521-528.
5
6. Bluming AZ, Tavris C. Hormone replacement therapy: real concerns and false alarms. Cancer J 2009; 15:93-104.
6
7. Chen CL, Weiss NS, Newcomb P, Barlow W, White E. Hormone replacement therapy in relation to breast cancer. Jama 2002; 287:734-741.
7
8. Mosca L, Collins P, Herrington DM, Mendelsohn ME, Pasternak RC, Robertson RM, et al. Hormone replacement therapy and cardiovascular disease a statement for healthcare professionals from the American Heart Association. Circulation 2001; 104:499-503.
8
9. Ososki AL, Kennelly EJ. Phytoestrogens: a review of the present state of research. Phytother Res 2003; 17:845-869.
9
10. Neves VJ, Fernandes T, Roque FR, Soci UPR, Melo SFS, de Oliveira EM. Exercise training in hypertension: Role of microRNAs. World J Cardiol 2014; 6:713.
10
11. Maillet M, van Berlo JH, Molkentin JD. Molecular basis of physiological heart growth: fundamental concepts and new players. Nat Rev Mol Cell Biol 2013; 14:38-48.
11
12. He L, Hannon GJ. MicroRNAs: small RNAs with a big role in gene regulation. Nat Rev Genet 2004; 5:522-531.
12
13. Small EM, Frost RJ, Olson EN. MicroRNAs add a new dimension to cardiovascular disease. Circulation 2010; 121:1022-1032.
13
14. Wang N, Sun LY, Zhang S-C, Wei R, Xie F, Liu J, et al. MicroRNA-23a participates in estrogen deficiency induced gap junction remodeling of rats by targeting GJA1. Int J Biol Sci 2015; 11:390.
14
15. Abdellatif M. The role of microRNA-133 in cardiac hypertrophy uncovered. Circul Res 2010; 106:16-18.
15
16. Wang H, Li J, Chi H, Zhang F, Zhu X, Cai J, et al. MicroRNA‐181c targets Bcl‐2 and regulates mitochondrial morphology in myocardial cells. J Cell Mol Med 2015; 19:2084-2097.
16
17. Irigoyen M-C, Paulini J, Flores LJ, Flues K, Bertagnolli M, Moreira ED, et al. Exercise training improves baroreflex sensitivity associated with oxidative stress reduction in ovariectomized rats. Hypertension 2005; 46:998-1003.
17
18. Da Silva Jr ND, Fernandes T, Soci U, Monteiro A, Phillips MI, de Oliveira EM. Swimming training in rats increases cardiac MicroRNA-126 expression and angiogenesis. Med Sci Sports Exerc 2012; 44:1453-1462.
18
19. Lv H, Sun Y, Zhang Y. MiR-133 is involved in estrogen deficiency-induced osteoporosis through modulating osteogenic differentiation of mesenchymal stem cells. Med Sci Monit 2015; 21:1527-1534.
19
20. Klinge CM. Estrogen regulation of microRNA expression. Curr Genom 2009; 10:169.
20
21. Kataoka M, Wang D-Z. Non-coding RNAs including miRNAs and lncRNAs in cardiovascular biology and disease. Cells 2014; 3:883-898.
21
22. Boštjančič E, Zidar N, Štajer D, Glavač D. MicroRNAs miR-1, miR-133a, miR-133b and miR-208 are dysregulated in human myocardial infarction. Cardiology 2010; 115:163-169.
22
23. Zhao H, Li M, Li L, Yang X, Lan G, Zhang Y. MiR-133b is down-regulated in human osteosarcoma and inhibits osteosarcoma cells proliferation, migration and invasion, and promotes apoptosis. PLoS One 2013; 8:e83571.
23
24. Care A, Catalucci D, Felicetti F, Bonci D, Addario A, Gallo P, et al. MicroRNA-133 controls cardiac hypertrophy. Nat Med 2007; 13:613-618.
24
25. He B, Xiao J, Ren AJ, Zhang YF, Zhang H, Chen M, et al. Role of miR-1 and miR-133a in myocardial ischemic postconditioning. J Biomed Sci 2011; 18:22.
25
26. Xu C, Lu Y, Pan Z, Chu W, Luo X, Lin H, et al. The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting HSP60, HSP70 and caspase-9 in cardiomyocytes. J Cell Sci 2007; 120:3045-3052.
26
27. Mitchelson KR, Qin WY. Roles of the canonical myomiRs miR-1,-133 and-206 in cell development and disease. World J Biol Chem 2015; 6:162.
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28. Xiao-Ming Y. Signal transduction mediated by Bid, a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways. Cell Res 2000; 10:161-167.
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29. Thomadaki H, Scorilas A. BCL2 family of apoptosis-related genes: functions and clinical implications in cancer. Crit Rev Clin Lab Sci 2006; 43:1-67.
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30. Pasiakos SM, McClung JP. miRNA analysis for the assessment of exercise and amino acid effects on human skeletal muscle. Adv Nutr 2013; 4:412-417.
30
31. Wang N, Zhou Z, Liao X, Zhang T. Role of microRNAs in cardiac hypertrophy and heart failure. IUBMB life 2009; 61:566-571.
31
32. Cheng SM, Ho TJ, Yang AL, Chen IJ, Kao CL, Wu FN, et al. Exercise training enhances cardiac IGFI-R/PI3K/Akt and Bcl-2 family associated pro-survival pathways in streptozotocin-induced diabetic rats. Int J Cardiol 2013; 167:478-485.
32
33. Huang CY, Yang AL, Lin YM, Wu FN, Lin JA, Chan YS, et al. Anti-apoptotic and pro-survival effects of exercise training on hypertensive hearts. J Appl Physiol 2012; 12:883-891.
33
ORIGINAL_ARTICLE
Assessment of oxidative stress parameters of brain-derived neurotrophic factor heterozygous mice in acute stress model
Objective(s): Exposing to stress may be associated with increased production of reactive oxygen species (ROS). Therefore, high level of oxidative stress may eventually give rise to accumulation of oxidative damage and development of numerous neurodegenerative diseases. It has been presented that brain-derived neurotrophic factor (BDNF) supports neurons against various neurodegenerative conditions. Lately, there has been growing evidence that changes in the cerebral neurotrophic support and especially in the BDNF expression and its engagement with ROS might be important in various disorders and neurodegenerative diseases. Hence, we aimed to investigate protective effects of BDNF against stress-induced oxidative damage. Materials and Methods: Five- to six-month-old male wild-type and BDNF knock-down mice were used in this study. Activities of catalase (CAT) and superoxide dismutase (SOD) enzymes, and the amount of malondialdehyde (MDA) were assessed in the cerebral homogenates of studied groups in response to acute restraint stress. Results: Exposing to acute physiological stress led to significant elevation in the markers of oxidative stress in the cerebral cortexes of experimental groups. Conclusion: As BDNF-deficient mice were observed to be more susceptible to stress-induced oxidative damage, it can be suggested that there is a direct interplay between oxidative stress indicators and BDNF levels in the brain.
https://ijbms.mums.ac.ir/article_6810_771e34e7ce67b1fdc8b36d6a7fe98078.pdf
2016-04-01
388
393
10.22038/ijbms.2016.6810
Brain-derived neurotrophic -factor
Cerebral cortex
Physiological stress
Reactive Oxygen Species
Gulay
Hacioglu
gulayhacioglu@yahoo.com
1
Department of Physiology, Faculty of Medicine, Giresun University, Turkey
LEAD_AUTHOR
Ayse
Senturk
asenturk@ktu.edu.tr
2
Department of Clinical Biochemistry, Faculty of Medicine, Karadeniz Technical University, Turkey
AUTHOR
Imran
Ince
narmince@hotmail.com
3
Department of Clinical Biochemistry, Faculty of Medicine, Karadeniz Technical University, Turkey
AUTHOR
Ahmet
Alver
alver61@yahoo.com
4
Department of Clinical Biochemistry, Faculty of Medicine, Karadeniz Technical University, Turkey
AUTHOR
1. Hong IS, Lee HY, Kim HP. Anti-oxidative effects of Rooibos tea (Aspalathus linearis) on immobilization-induced oxidative stress in rat brain. PLoS One 2014; 21 9:e87061.
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2. Kelly GS. Nutritional and botanical interventions to assist with the adaptation to stress. Altern Med Rev 1999; 4:249-265.
2
3. Liu J, Mori A. Stress, aging, and brain oxidative damage. Neurochem Res 1999; 24:1479-1497.
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4. Uttara B, Singh AV, Zamboni P, Mahajan RT. Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Curr Neuropharmacol 2009; 7:65-74.
4
5. Huang EJ, Reichardt LF. Trk receptors: roles in neuronal signal transduction. Annu Rev Biochem 2003; 72:609-642.
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6. Numakawa T, Suzuki S, Kumamaru E, Adachi N, Richards M, Kunugi H. BDNF function and intracellular signaling in neurons. Histol Histopathol 2010; 25:237-258.
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7. Vedunova MV, Mishchenko TA, Mitroshina EV, Mukhina IV. TrkB-mediated neuroprotective and antihypoxic properties of brain-derived neurotrophic factor. Oxid Med Cell Longev 2015; 2015:453901.
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8. Numakawa T, Matsumoto T, Numakawa Y, Richards M, Yamawaki S, Kunugi H. Protective action of neurotrophic factors and estrogen against oxidative stress-mediated neurodegeneration. J Toxicol 2011; 2011:405194.
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9. Ferrer I, Goutan E, Marín C, Rey MJ, Ribalta T. Brain-derived neurotrophic factor in Huntington disease. Brain Res 2000; 866:257-261.
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10. Gines S, Seong IS, Fossale E, Ivanova E, Trettel F, Gusella JF, et al. Specific progressive cAMP reduction implicates energy deficit in presymptomatic Huntington's disease knock-in mice. Hum Mol Genet 2003; 12:497-508.
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11. Counts SE, Mufson EJ. Noradrenaline activation of neurotrophic pathways protects against neuronal amyloid toxicity. J Neurochem 2010; 113:649-660.
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12. Giese M, Unternaehrer E, Brand S, Calabrese P, Holsboer-Trachsler E, Eckert A. The interplay of stress and sleep impacts BDNF level. PLoS One 2013; 16 8(10):e76050.
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13. Aydemir O, Deveci A. BDNF measurement in stress-related mood disorders: a review of clinical studies. Turk Psikiyatri Derg 2009; 20:385-391.
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14. Duman RS. Pathophysiology of depression: the concept of synaptic plasticity. Eur Psychiatry 2002; 17:306S-310S.
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15. Pae CU, Chiesa A, Porcelli S, Han C, Patkar AA, Lee SJ, et al. Influence of BDNF variants on diagnosis and response to treatment in patients with major depression, bipolar disorder and schizophrenia. Neuropsychobiology 2011; 65:1-11.
15
16. Haghighi M, Salehi I, Erfani P, Jahangard L, Bajoghli H, Holsboer-Trachsler E, et al. Additional ECT increases BDNF-levels in patients suffering from major depressive disorders compared to patients treated with citalopram only. J Psychiatr Res 2013; 47:908-915.
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17. Hosang GM, Shiles C, Tansey KE, McGuffin P, Uher R. Interaction between stress and the BDNF Val66Met polymorphism in depression: a systematic review and meta-analysis. BMC Med 2014; 16 12:7.
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18. Tsuru J, Tanaka Y, Ishitobi Y, Maruyama Y, Inoue A, Kawano A, et al. Association of BDNF Val66Met polymorphism with HPA and SAM axis reactivity to psychological and physical stress. Neuropsychiatr Dis Treat 2014; 11:2123-2133.
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19. Burke TF, Advani T, Adachi M, Monteggia LM, Hensler JG. Sensitivity of hippocampal 5-HT1A receptors to mild stress in BDNF-deficient mice. Int J Neuropsychopharmacol 2013; 16:631-645.
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20. Korte M, Carroll P, Wolf E, Brem G, Thoenen H, Bonhoeffer T. Hippocampal long-term potentiation is impaired in mice lacking brain-derived neurotrophic factor. Proc Natl Acad Sci U S A 1995; 92:8856-8860.
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21. Abidin I, Eysel UT, Lessmann V, Mittmann T. Impaired GABAergic inhibition in the visual cortex of brain-derived neurotrophic factor heterozygous knockout mice. J Physiol 2008; 586:1885-1901.
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27. Landis GN, Tower J. Superoxide dismutase evolution and life span regulation. Mech Ageing Dev 2005; 126:365-379.
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28. Al-Abrash AS, Al-Quobaili FA, Al-Akhras GN. Catalase evaluation in different human diseases associated with oxidative stress. Saudi Med J 2000; 21:826-830.
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29. Abidin I, Köhler T, Weiler E, Zoidl G, Eysel UT, Lessmann V, et al. Reduced presynaptic efficiency of excitatory synaptic transmission impairs LTP in the visual cortex of BDNF-heterozygous mice. Eur J Neurosci 2006; 24:3519-3531.
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30. Sahin E, Gümüşlü S. Immobilization stress in rat tissues: alterations in protein oxidation, lipid peroxidation and antioxidant defense system. Comp Biochem Physiol C Toxicol Pharmacol 2007; 144:342-347.
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40. Gama CS, Berk M, Andreazza AC, Kapczinski F, Belmonte-de-Abreu P. Serum levels of brain-derived neurotrophic factor and thiobarbituric acid reactive substances in chronically medicated schizophrenic patients: a positive correlation. Rev Bras Psiquiatr 2008; 30:337-340.
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44
ORIGINAL_ARTICLE
The effect of spinally administered WIN 55,212-2, a cannabinoid agonist, on thermal pain sensitivity in diabetic rats
Objective(s):Diabetic neuropathy (DN) is a common complication of diabetes that leads to allodynia, impaired nerve conduction, and progressive sensory loss. The aim of this study was to observe the effect of a high-affinity cannabinoid receptors agonist, WIN 55,212-2, on thermal hyperalgesia, nerve conduction velocity and sciatic nerve histopathology in diabetic rats.
Materials and Methods: Diabetes was induced in rats using a single dose of streptozotocin (45 mg/kg IP).
Results: Intrathecal (IT) administration of WIN55, 212-2 (1, 10, 100 µg/10 µl, IT), produced antinociceptive effects in the hot plate test and also improved nerve conduction velocity (100 µg/10 µl, IT) and sciatic nerve histology.
Conclusion: These data show that cannabinoids have potent antinociceptive effects through direct actions in the spinal dorsal horn of nociceptive pathway. This suggests that intrathecally administered cannabinoids may offer hopeful strategies for the treatment of diabetic neuropathic pain.
https://ijbms.mums.ac.ir/article_6811_421360aa137ac61c02d71638a29b5b98.pdf
2016-04-01
394
401
10.22038/ijbms.2016.6811
Diabetes
Intrathecal
Neuropathy
Pain
WIN 55
212-2
Samane
Jahanabadi
1
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mohamad Reza
Hadian
hadianrs@sina.tums.ac.ir
2
Department of Physical Therapy, Faculty of Rehabilitation Sciences, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Javad
Shamsaee
jshamsaee@yahoo.com
3
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Mohammad
Tavangar
4
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Alireza
Abdollahi
alireza.a1345@yahoo.com
5
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ahmadreza
Dehpour
dehpour@medscuape.com
6
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shahram
Ejtemaei Mehr
ejtemam@gmail.com
7
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Hohmann AG,Tsou K, Walker JM. Cannabinoid modulation of wide dynamic range neurons in the lumbar dorsal horn of the rat by spinally administered WIN55,212-2. Neurosci Lett 1998; 257:119-122.
1
2. Fox A, Kesingland A, Gentry C, McNair K, Patel S, UrbanL, et al. The role of central and peripheral cannabinoid 1 receptors in the antihyperalgesic activity of cannabinoids in a model of neuropathic pain. Pain 2001; 92:91-100.
2
3. Tsou K, Brown S, Sanudo-Pena M, Mackie K, Walker J. Immunohistochemical distribution of cannabinoid CB1 receptors in the rat central nervous system. Neuroscience 1998; 83:393-411.
3
4. Hohmann A, Herkenham M. Localization of central cannabinoid CB1 receptor messenger RNA in neuronal subpopulations of rat dorsal root ganglia: a double-label in situ hybridization study. Neuroscience 1999; 90:923-931.
4
5. Hohmann A, Herkenham M. Cannabinoid receptors undergo axonal flow in sensory nerves. Neuroscience 1999; 92:1171-1175.
5
6. Martin WJ, Loo CM, Basbaum AI. Basbaum, Spinal cannabinoids are anti-allodynic in rats with persistent inflammation. Pain 1999; 82:199-205.
6
7. Li J, Daughters RS, Bullis C, Bengiamin R, Stucky MW, Brennan J, et al. The cannabinoid receptor agonist WIN 55,212-2 mesylate blocks the development of hyperalgesia produced by capsaicin in rats. Pain 1999; 81:25-33.
7
8. Costa B, Siniscalco D, Trovato AE, Comelli F, Sotgiu ML, Colleoni M, et al. AM404, an inhibitor of anandamide uptake, prevents pain behaviour and modulates cytokine and apoptotic pathways in a rat model of neuropathic pain. Br J Pharmacol 2006; 148:1022-1032.
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9. Liang YC, Huang CC, Hsu KS. The synthetic cannabinoids attenuate allodynia and hyperalgesia in a rat model of trigeminal neuropathic pain. Neuropharmacology 2007; 53:169-177.
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10. Siegling A, Hofmann HA, Denzer D, Mauler F, De Vry J. Cannabinoid CB 1 receptor upregulation in a rat model of chronic neuropathic pain. Eur J Pharmacol 2001; 415:R5-R7.
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11. Bridges D, Thompson S, Rice A. Mechanisms of neuropathic pain. Br J Anaesth 2001; 87:12-26.
11
12. Pertwee RG. Cannabis and cannabinoids: pharmacology and rationale for clinical use. Forsch Komplementarmed 1999; 6:12-15.
12
13. Rice A, Farquhar-Smith W, Nagy I. Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy. Prostaglandins Leukot Essent Fatty Acids 2002; 66:243-256.
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14. Vaughan CW, Christie MJ. An analgesic role for cannabinoids. Med J Australia 2000; 173:270-272.
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15. Scott DA, Wright CE, Angus JA. Evidence that CB-1 and CB-2 cannabinoid receptors mediate antinociception in neuropathic pain in the rat. Pain 2004; 109:124-131.
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55
ORIGINAL_ARTICLE
Effect of carvacrol on various cytokines genes expression in splenocytes of asthmatic mice
Objective(s):With regard to pharmacological effects of carvacrol on the respiratory system, its effect on cytokines genes expression in splenocytes of asthmatic mice was examined in this study.
Materials and Methods:Splenocytes were isolated from non-sensitized (control group), sensitized mice to ovalbumin (OVA) (group S), and S animals treated with dexamethasone, and three concentrations of carvacrol. IL-4, IFN-γ, TGF-β, FOXP3, and IL-17 genes expression were carried out in cultured splenocytes using the real-time PCR method.
Results:Compared to the control group, IFN-γ and FOXP3 genes expression were significantly decreased (P<0.001 for both cases), but IL-4 and IL-17 genes expression were significantly increased in the S group (P<0.001 and P<0.05, respectively). IL-4 gene expression due to treatment of all concentrations of carvacrol, TGF-β gene expression due to its two higher concentrations, and IL-17 gene expression due to its high concentration were significantly decreased compared to group S (P<0.01 to P<0.001). IFN-γ gene expression was significantly increased due to last carvacrol concentration (300 µg/ml, P<0.01), and FOXP3 due to its two last concentrations (150 and 300 µg/ml, P<0.05 and P<0.001, respectively) in treated S splenocytes. Dexamethasone treatment of sensitized splenocytes only showed significant inhibitory effect on IL-4 and TGF-β genes expression (P<0.001 for both cases).
Conclusion: These results showed the immunomodulatory effect of carvacrol indicating increased IFN-γ and FOXP3 but decreased IL-4, TGF-β, and IL-17 genes expression, which was more selective than the effect of dexamethasone in sensitized mice splenocytes, which indicates its possible therapeutic value in allergy, autoimmunity, and infectious diseases.
https://ijbms.mums.ac.ir/article_6812_0ac3fede8d1a9cc1029dd0408aeb3570.pdf
2016-04-01
402
410
10.22038/ijbms.2016.6812
Carvacrol
Cytokines
Gene expression
Real-time PCR
Splenocyte
Majid
Kianmehr
kianmehrm891@mums.ac.ir
1
Neurogenic Inflammation Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Abdolrahim
Rezaei
2
Inflammation and Inflammatory Diseases Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad Hossein
Boskabady
boskabadymh@mums.ac.ir
3
Neurogenic Inflammation Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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52
ORIGINAL_ARTICLE
Quinazoline derivative compound (11d) as a novel angiogenesis inhibitor inhibiting VEGFR2 and blocking VEGFR2-mediated Akt/mTOR /p70s6k signaling pathway
Objective(s): We previously reported a series of quinazoline derivatives as vascular-targeting anticancer agents. In this study, we investigated the mechanism underlying the anti-angiogenic activity of the quinazoline derivative compound 11d.
Materials and Methods: We examined the effects of quinazoline derivative 11d on vascular endothelial growth factor receptor-2 (VEGFR2) activation via VEGFR2-specific activation assay. Reverse transcription and immunohistochemistry were used to detect vascular endothelial growth factor (VEGF), VEGFR2, and the VEGFR2-mediated Akt/mTOR/p70s6k signaling pathway in human umbilical vascular endothelial cells and hepatocellular carcinoma cells (HepG-2) after treatment with various concentrations of 11d (0, 6.25, 12.5, and 25 μM) for 24 hr.
Results: The compound 11d exhibited potent inhibitory activity against VEGFR2 with an IC50 of 5.49 μM. This compound significantly downregulated VEGF, VEGFR2, and the VEGFR2-mediated Akt/mTOR/p70s6k signaling pathway in vitro.
Conclusion:The mechanism underlying the anti-angiogenic activity of the quinazoline derivative 11d possibly involves the inhibition of VEGFR2 and the downregulation of VEGF, VEGFR2, and the VEGFR2-mediated Akt/mTOR/p70s6k signaling pathway. Overall, the findings indicate that the studied class of compounds is a source of potential antiproliferative and anti-angiogenic agents, which must be further investigated.
https://ijbms.mums.ac.ir/article_6813_9d85d0e6f2dc562b4ee1095e18163132.pdf
2016-04-01
411
416
10.22038/ijbms.2016.6813
anti-angiogenic Akt/mTOR/p70s6k mechanism
Quinazoline derivatives
VEGF
VEGFR2
Zeng
Li
zongshengyin1314@sina.com
1
Department of Pharmacy, Anhui Medical University, Hefei 230032, China
AUTHOR
Bin
Wang
2
Department of Pharmacy, Xiangnan University, Chenzhou 423000, China
AUTHOR
Liang
Tang
tang@163.com
3
Department of Chirurgery, First Affiliated Hospital of Anhui Medical University, Hefei 230032, China
AUTHOR
Shuangsheng
Chen
chenshuangs163126@163.com
4
Department of Pharmacy, Anhui Medical University, Hefei 230032, China
AUTHOR
Jun
Li
zongshengyin1314@163.com
5
Department of Pharmacy, Anhui Medical University, Hefei 230032, China
LEAD_AUTHOR
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24. Li W, Tan D, Zhang Z, et al. Activation of Akt-mTOR-p70S6K pathway in angiogenesis in hepatocellular carcinoma. Oncol Rep 2008; 204: 713-719.
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25. Ciuffreda L, Di Sanza C, Incani, UC, et al. The mTOR pathway: a new target in cancer therapy. Curr Cancer Drug Targets 2010; 10: 484-49.
25
26. Bian CX, Shi Z, Meng Q. P70S6K 1 regulation of angiogenesis through VEGF and HIF-1alpha expression. Biochem Biophys Res Commun 2010; 398: 395-399.
26
ORIGINAL_ARTICLE
Naringin ameliorates cognitive deficits in streptozotocin-induced diabetic rats
Objective(s):Previous research demonstrated that diabetes is one of the leading causes of learning and memory deficits. Naringin, a bioflavonoid isolated from grapefruits and oranges, has potent protective effects on streptozotocin (STZ)-induced diabetic rats. Recently, the effects of naringin on learning and memory performances were monitored in many animal models of cognitive impairment. However, to date, no studies have investigated the ameliorative effects of naringin on diabetes-associated cognitive decline (DACD). In this study, we investigated the effects of naringin, using a STZ-injected rat model and explored its potential mechanism. Materials and Methods:Diabetic rats were treated with naringin (100 mg/kg/d) for 7 days. The learning and memory function were assessed by Morris water maze test. The oxidative stress indicators [superoxide dismutase (SOD) and malondialdehyde (MDA)] and inflammatory cytokines (TNF-a, IL-1β, and IL-6) were measured in hippocampus using corresponding commercial kits. The mRNA and protein levels of PPARγ were evaluated by real time (RT)-PCR and Western blot analysis. Results:The results showed that supplementation of naringin improved learning and memory performances compared with the STZ group. Moreover, naringin supplement dramatically increased SOD levels, reduced MDA levels, and alleviated TNF-α, IL-1β, and IL-6 compared with the STZ group in the hippocampus. The pretreatment with naringin also significantly increased PPARγ expression. Conclusion: Our results showed that naringin may be a promising therapeutic agent for improving cognitive decline in DACD.
https://ijbms.mums.ac.ir/article_6814_d71e3e0f47caa92c077f2b66ba92bcc1.pdf
2016-04-01
417
422
10.22038/ijbms.2016.6814
Cognitive
DACD
Inflammation
Naringin
Oxidative stress
PPARγ
Xianchu
Liu
1
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Ming
Liu
liuminglinxi@163.com
2
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Yanzhi
Mo
3
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Huan
Peng
4
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Jingbo
Gong
5
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Zhuang
Li
6
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Jiaxue
Chen
7
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
AUTHOR
Jingtao
Xie
xiejingtao516@163.com
8
Department of Applied Psychology, Hunan University of Chinese Medicine, Hunan, PR China
LEAD_AUTHOR
1. Gispen WH, Biessels GJ. Cognition and synaptic plasticity in diabetes mellitus. Trends Neurosci 2000; 23:542-549.
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2. Biessels GJ, Kappelle AC, Bravenboer B, Erkelens DW, Gispen WH. Cerebral function in diabetes mellitus. Diabetologia 1994; 37:643-650.
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3. Mijnhout GS, Scheltens P, Diamant M, Biessels GJ, Wessels AM, Simsek S, Snoek FJ, Heine RJ. Diabetic encephalopathy: A concept in need of a definition. Diabetologia 2006; 49:1447-1448.
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4. Kodl CT, Seaquist ER. Cognitive dysfunction and diabetes mellitus. Endocr Rev 2008; 29:494-511.
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5. Li WA, Moore-Langston S, Chakraborty T, Rafols JA, Conti AC, Ding Y. Hyperglycemia in stroke and possible treatments. Neurol Res 2013; 35:479-491.
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6. Harada S, Fujita-Hamabe W, Tokuyama S. Ameliorating effect of hypothalamic brain-derived neurotrophic factor against impaired glucose metabolism after cerebral ischemic stress in mice. J Pharmacol Sci 2012; 118:109-116.
6
7. Morabito MV, Berman DE, Schneider RT, Zhang Y, Leibel RL, Small SA. Hyperleucinemia causes hippocampal retromer deficiency linking diabetes to Alzheimer's disease. Neurobiol Dis 2014; 65:188-192.
7
8. Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006; 444:860-867.
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9. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O, Makishima M, Matsuda M, Shimomura I. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest 2014; 114:1752-1761.
9
10. Feng X, Gao X, Jia Y, Zhang H, Pan Q, Yao Z, Yang N, Liu J, Xu Y, Wang G, Yang X. PPAR-α agonist fenofibrate decreased serum irisin levels in type 2 diabetes patients with hypertriglyceridemia. PPAR Res 2015; 501:924131.
10
11. Saito T, Hasegawa-Moriyama M, Kurimoto T, Yamada T, Inada E, Kanmura Y. Resolution of inflammation by resolvin D1 is essential for peroxisome proliferator–activated receptor-γ–mediated analgesia during postincisional pain development in type 2 diabetes. J Am Soc Anesthesiol 2015; 123:1420-1434.
11
12. Lee TI, Kao YH, Chen YC, Pan NH, Lin YK, Chen YJ. Cardiac peroxisome-proliferator-activated receptor expression in hypertension co-existing with diabetes. Clin Sci 2011; 121:305-312.
12
13. Pereira RM, Andrades NE, Paulino N, Sawaya AC, Eberlin MN, Marcucci MC, Favero GM, Novak EM, Bydlowski SP. Synthesis and characterization of a metal complex containing Naringin and Cu, and its antioxidant, antimicrobial, antiinflammatory and tumor cell cytotoxicity. Molecules 2007; 12:1352-1366.
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14. Cui L, Zhang ZH, Sun E, Jia XB. Effect of β-cyclodextrin complexation on solubility and enzymatic conversion of naringin. Int J Mol Sci 2012; 13:14251-14261.
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15. Wang DM, Yang YJ, Zhang L, Zhang X, Guan FF, Zhang LF. Naringin Enhances CaMKII Activity and Improves Long-Term Memory in a Mouse Model of Alzheimer's Disease. Int J Mol Sci 2013; 14:5576-86.
15
16. Prakash A, Shur B, Kumar A. Naringin protects memory impairment and mitochondrial oxidative damage against aluminum-induced neurotoxicity in rats. Int J Neurosci 2013; 123:636-645.
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17. Wang D, Gao K, Li X, Shen X, Zhang X, Ma C, Qin C, Zhang L. Long-term Naringin consumption reverses a glucose uptake defect and improves cognitive deficits in a mouse model of Alzheimer's disease. Pharmacol Biochem Behav 2012; 102:13-20.
17
18. Golechha M, Chaudhry U, Bhatia J, Saluja D, Arya DS. Naringin protects against kainic acid-induced status epilepticus in rats: evidence for an antioxidant, anti-inflammatory and neuroprotective intervention. Biol Pharm Bull 2011; 34:360-365.
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19. Zhang M, Lv XY, Li J, Xu ZG, Chen L. The characterization of high-fat diet and multiple low-dose streptozotocin induced type 2 diabetes rat model. Exp Diabetes Res 2008; 2008:704045.
19
20. Li R, Zang A, Zhang L, Zhang H, Zhao L, Qi Z, Wang H. Chrysin ameliorates diabetes-associated cognitive deficits in Wistar rats. Neurol Sci 2014; 35:1527-1532.
20
21. Hakeem P, Sani HA, Noor MM. Effects of gynura procumbens extract and glibenclamide on sperm quality and specifc activity of testicular lactate dehydrogenase in streptozotocin-induced diabetic rats. J Complement Integr Med 2015; 16:10-14.
21
22. Sharma AK, Bharti S, Ojha S, Bhatia J, Kumar N, Ray R, Kumari S, Arya DS. Up-regulation of PPARγ, heat shock protein-27 and -72 by Naringin attenuates insulin resistance, β-cell dysfunction, hepatic steatosis and kidney damage in a rat model of type 2 diabetes. Br J Nutr 2011; 106:1713-1723.
22
23. Kandhare AD, Raygude KS, Ghosh P, Ghule AE, Bodhankar SL. Neuroprotective effect of naringin by modulation of endogenous biomarkers in streptozotocin induced painful diabetic neuropathy. Fitoterapia 2012; 83:650-659.
23
24. Fukui K, Onodera K, Shinkai T, Suzuki S, Urano S. Impairment of learning and memory in rats caused by oxidative stress and aging, and changes in antioxidative defense systems. Ann N Y A Sci 2001; 928:168-175.
24
25. Liu YW, Zhu X, Li W, Lu Q, Wang JY, Wei YQ, Yin XX. Ginsenoside reattenuates diabetes-associated cognitive deficits in rats. Pharm Biochem Behav 2012; 101:93-98.
25
26. Deng W, Lu H, Teng J. Carvacrol attenuates diabetes-associated cognitive deficits in rats. J Mol Neurosci 2013; 51:813-819.
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27. Sood V, Colleran K, Burge MR. Thiazolidinediones: a comparative review of approved uses. Diabetes Technol Ther 2000; 2:429-440.
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28. Kemnitz JW, Elson DF, Roecker EB, Baum ST, Bergman RN, Meglasson MD. Pioglitazone increases insulin sensitivity, reduces blood glucose, insulin, and lipid levels, and lowers blood pressure in obese, insulin-resistant Rhesus monkeys. Diabetes 1994; 43: 204-211.
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29. Gumieniczek A. Effect of the new thiazolidine- dione-pioglitazone on the development of oxidative
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stress in liver and kidney of diabetic rabbits. Life Sci 2003; 74:553-562.
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30. Jahrling JB, Hernandez CM, Denner L, Dineley KT. PPARγ recruitment to active ERK during memory consolidation is required for Alzheimer's disease-relatedcognitive enhancement. J Neurosci 2014; 34:4054-63.
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31. Liu LP, Yan TH, Jiang LY, Hu W, Hu M, Wang C, Zhang Q, Long Y, Wang JQ, Li YQ, Hu M, Hong H. Pioglitazone ameliorates memory deficits in streptozotocin-induced diabetic mice by reducing brain β-amyloid through PPAR γ activation. Acta Pharmacol Sin 2013; 34: 455-463.
32
ORIGINAL_ARTICLE
Inhibitory effect of clemastine on P-glycoprotein expression and function: an in vitro and in situ study
Objective(s):Transporters have an important role in pharmacokinetics of drugs. Inhibition or induction of drug transporters activity can affect drug absorption, safety, and efficacy. P-glycoprotein (P-gp) is the most important membrane transporter that is responsible for active efflux of drugs. It is important to understand which drugs are substrates, inhibitors, or inducers of P-gp to minimize or avoid unwanted interactions. The aim of this study was to investigate the effects of clemastine on the expression and function of P-gp.
Materials and Methods: The effect of clemastine on P-gp function and expression was evaluated in vitro byrhodamine-123 (Rho123) efflux assay in Caco-2 cells and Western blot analysis. Rat in situ single pass intestinal permeability model was used to investigate the clemastine effect on digoxin Peff, as a known P-gp substrate. Digoxin levels in intestinal perfusates were assayed by high performance liquid chromatography (HPLC) method.
Results:The Caco-2 intracellular accumulation of Rho123 in clemastine and verapamil treated cells was 90.8 ± 9.8 and 420.6±25.4 pg/mg protein, respectively which was significantly higher than that in control cells (50.2±6.0; P<0.05). Immunoblotting results indicated that clemastine decreased expression of P-gp in Caco-2 cells in vitro. More over effective intestinal permeability (Peff) of digoxin in the presence of clemastine, was significantly increased compare to control group.
Conclusion: Findings of our study suggested dose dependent P-gp inhibition activity for clemastine in vitro and in situ. Therefore co-administration of clemastine with P-gp substrates may result in unwanted interactions and side effects.
https://ijbms.mums.ac.ir/article_6815_563c9975ba66430234720970c3946166.pdf
2016-04-01
423
429
10.22038/ijbms.2016.6815
Clemastine
Digoxin
Intestinal Absorption
P-glycoprotein
Mehran
Mesgari Abbasi
mesgarim@tbzmed.ac.ir
1
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Hadi
Valizadeh
valizadeh@tbzmed.ac.ir
2
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Hamed
Hamishekar
parvinzm@gmail.com
3
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Leila
Mohammadnejad
4
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Parvin
Zakeri-Milani
pzakeri@tbzmed.ac.ir
5
Liver and Gastrointestinal Diseases Research Center and Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1. Lumen AA, Li L, Li J, Ahmed Z, Meng Z, Owen A, et al. Transport inhibition of digoxin using several common P-gp expressing cell lines is not necessarily reporting only on inhibitor binding to P-gp. PLoS One 2013; 8:e69394.
1
2. Kishimoto W, Ishiguro N, Ludwig-Schwellinger E, Ebner T, Schaefer O. In Vitro predictability of drug-drug interaction likelihood of P-glycoprotein-mdiated efflux of dabigatran etexilate based on [I]2/IC50 threshold. Drug Metab Dispos 2014; 42:257–263.
2
3. Kobori T, Harada S, Nakamoto K, Tokuyama S. Mechanisms of P-glycoprotein alteration during anticancer treatment: role in the pharmacokinetic and pharmacological effects of various substrate drugs. J Pharmacol Sci 2014; 125:242–254.
3
4. Kobori T, Harada S, Nakamoto K, Tokuyama S. Functional alterations of intestinal P-glycoprotein under diabetic conditions. Biol Pharm Bull 2013; 36:1381–1390.
4
5. Li Y, Huang L, Zeng X, Zhong G, Ying M, Huang M, et al. Down-regulation of P-gp expression and function after mulberroside a treatment: potential role of protein kinase C and NF-kappa B. Chem Biol Interact 2014; 213:44–50.
5
6. Wessler JD, Grip LT, Mendell J, Giugliano RP. The P-glycoprotein transport system and cardiovascular drugs. J Am Coll Cardiol 2013; 61:2495–2502.
6
7. Han S, Karłowicz-Bodalska K, Miśkiewicz K, Kutycka E, Kuchar E. Safety of oral clemastine–analysis of data from spontaneous reporting system in poland. Trop J Pharm Res 2014; 13:2115-2118.
7
8. Tevell A, Bondesson U, Tourneke K, Hedeland M. Identification of some new clemastine metabolites in dog, horse, and human urine with liquid chromatography/tandem mass spectrometry. Rapid Commun Mass Spectrom 2004; 18:2267–2272.
8
9. Minigh J. Clemastine. xPharm: The Comprehensive Pharmacology Reference 2008;1–6.
9
10. Han y, Chin Tan TM, Lim L. In vitro and in vivo evaluation of the effects of piperine on P-gp function and expression. Toxicol Appl Pharmacol 2008; 230:283-289.
10
11. Zrieki A, Farinotti R, Buyse M. Cyclooxygenase-2 inhibitors prevent trinitrobenzene sulfonic acid-induced P-glycoprotein up-regulation in vitro and in vivo. Eur J Pharmacol 2010; 636:189–197.
11
12. Zastrea J, Jacksona J, Bajwaa M, Ligginsb R, Iqbala F, Burta H. Enhanced cellular accumulation of a P-glycoprotein substrate, rhodamine-123, by caco-2 cells using low molecular weight methoxypolyethylene glycol-block-polycaprolactone diblock copolymers. Eur J Pharm Biopharm 2002; 54:299–309.
12
13. Wanga XD, Menga MX, Gaoa LB, Liua T, Xub Q, Zenga S. Permeation of astilbin and taxifolin in Caco-2 cell and their effects on the P-gp. Int J Pharm 2009; 378:1–8.
13
14. Patel JR, Barve KH. Intestinal permeability of lamivudine using single pass intestinal perfusion. Indian J Pharm Sci 2012; 74:478–481.
14
15. Zakeri-Milani P, Valizadeh H, Tajerzadeh H, Azarmi Y, Islambolchilar Z, Barzegar S, et al. Predicting human intestinal permeability using single-pass intestinal perfusion in rat. J Pharm Pharm Sci 2007; 10:368-379.
15
16. Valizadeh H, Mehtari M, Zakeri-Milani P. Evidence for enhanced intestinal absorption of digoxin by P-glycoprotein inhibitors. Trop J Pharm Res 2012; 11:939-945.
16
17. Prasad N, Bhasker S. Characterization of intestinal transport of Vincristine in rats applying in situ single pass intestinal perfusion. Pharmacologia 2012; 3:617-621.
17
18. Broccatellia F, Carosatia E, Nerib A, Frosinib M, Goraccic L, Opread TI, et al. A novel approach for predicting P-glycoprotein (ABCB1) inhibition using molecular interaction fields. J Med Chem 2011; 54:1740–1751.
18
19. Shityakov S, Förster C. In silico structure-based screening of versatile P-glycoprotein inhibitors using polynomial empirical scoring functions. Adv Appl Bioinform Chem 2014; 7:1–9.
19
20. Obradovic T, Dobson GG, Shingaki T, Kungu T, Hidalgo IJ. Assessment of the first and second generation antihistamines brain penetration and role of P-glycoprotein. Pharm Res 2007; 24:318-327.
20
21.Varma MVS, Sateesh K, Panchagnula R. Functional role of P-glycoprotein in limiting intestinal absorption of drugs: contribution of passive permeability to P-glycoprotein mediated efflux transport. Mol Pharm 2004; 2:2-21.
21
22. Wessler JD, Grip LT, Mendell J, Giugliano RP. The P-glycoprotein transport system and cardiovascular drugs. J Am Coll Cardiol 2013; 61:2495–2502.
22
23. Drug information online, http://www. drugs.com/-cdi/clemastine.html
23
24. Zakeri-Milani P, Valizadeh H. Intestinal transporters: enhanced absorption through P-glycoprotein-related drug interactions. Expert Opin Drug Metab Toxicol 2014; 10:859-871.
24
ORIGINAL_ARTICLE
Evaluation of antioxidant and cytoprotective activities of Artemisia ciniformis extracts on PC12 cells
Objective(s): In the current study antioxidant capacities of five different extracts of Artemisia ciniformis aerial parts were evaluated by cell-free methods. Then seven fractions of the potent extract were selected and their antioxidant capacity was assayed by cell free and cell based methods.
Materials andMethods: Antioxidant ability was measured using the: 2, 2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging test, β-carotene bleaching (BCB) method and ferrous ion chelating (FIC) assay. Total phenolic contents (TPC) of all the samples also were determined. The cytoprotective effect of fractions was evaluated by measuring the viability of cells after exposure to doxorubicin (DOX). The mechanism of action was studied by investigating caspase-3, mitochondrial membrane potential (MMP), the level of super-oxide dismutase (SOD) and intracellular reactive oxygen species (ROS).
Results: Hydroethanolic extract exhibited a notably higher antioxidant activity and phenolic content. Among the fractions (A to G) of hydroethanolic extract, the highest antioxidant capacity was observed in the Fraction E. Moreover, 24 hr pretreatment of PC12 cells with fractions B, C and D decreased DOX-induced cytotoxicity. In addition, pre-treatment of cells with fraction B resulted in significant decrease in generation of the reactive oxygen species (ROS) and increase in the activity of SOD. We were able to demonstrate remarkable reduction in the activity of caspase-3 and increase in MMP in PC12 cells following pretreatment with fraction B.
Conclusion: Our observations indicated that the fraction B of A. ciniformis hydroetanolic extract possessed protective effect on oxidative stress and apoptosis induced by DOX in PC12 cells.
https://ijbms.mums.ac.ir/article_6816_7d4a45759c81207d556565dc31704d9f.pdf
2016-04-01
430
438
10.22038/ijbms.2016.6816
Apoptosis
Artemisia ciniformis
Oxidative stress
PC12 cell line
Mahdi
Mojarrab
mmojarrab@kums.ac.ir
1
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Sajjad
Nasseri
sajjadnaseri66@yahoo.com
2
Students Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Leila
Hosseinzadeh
ladan.hoseinzadeh@gmail.com
3
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
LEAD_AUTHOR
Farah
Farahani
frahfarahinfo@gmail.com
4
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
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45. Kanhere R, Anjana A, Anbu J. Neuroprotective and antioxidant potential of terpenoid fraction from Hygrophila auriculata against transient global cerebral ischemia in rats. Pharm Biol 2013; 51:181-189.
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48. Kim YC. Neuroprotective phenolics in medicinal plants. Arch Pharmacol Res 2010; 33:1611-1632.
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50. Zhang W, Wang J, Jin W, Zhang Q. The antioxidant activities and neuroprotective effect of polysaccharides from the starfish Asteriasrollestoni. Carbohyd Polym 2013; 5:95:9-15.
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51. Shi J, Li CJ, Yang JZ, Yuan YH, Chen MH, Zhang DM. Coumarin glycosides and iridoidGlucosides with neuroprotective effects from hydrangea paniculata. Planta Med 2012; 78:1844-1850.
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53. Sarvestani NN, Khodagholi F, Ansari N, Farimini MN. Involvement of p-CREB and phase II detoxifying enzyme system in neuroprotection mediated by the flavonoid calycopterin isolated from Dracocephalumkotschyi. Phytomedicine 2013; 20:939-946.
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55. Hu W, Wang G, Li P, Wang Y, Si CL, He J, et al. Antioxidant properties and neuroprotective effects of isocampneoside II on hydrogen peroxide-induced oxidative injury in PC12 cells. Food Chem Toxicol 2013; 59:145-152.
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56. Jin W, Zhang W, Wang J, Zhang Q. The neuroprotective activities and antioxidant activities of the polysaccharides fromSaccharina japonica. Int J Biol Macromol 2013; 58:240-244.
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57. Ji X, Rivers L, Zielinski, MacDugal E, Jancy S, Zhang S. Quantitative analysis of phenolic components and glycoalkaloids from 20 potato clones and in vitro evaluation of antioxidant, cholesterol uptake, and neuroprotective activities. Food Chem 2011; 133:1177-1188.
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58. Naik GH, Priyadarsini KI, Satav JG, Banavalikar MM, Sohoni DP, Biyani MK, et al. Comparative antioxidant activity of individual herbal components used in Ayurvedic medicine. Phytochemistry 2003; 63:97–104.
58
59. Djidel S, khennouf S. Radical scavenging, reducing power, lipid peroxidation inhibition and chelating properties of extracts froma artemisia campestris L. Aerial Parts. Ann Res Rev Biol 2014; 4:1691-1702.
59
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60
ORIGINAL_ARTICLE
Brain-derived neurotrophic and immunologic factors: beneficial effects of riboflavin on motor disability in murine model of multiple sclerosis
Objective(s): In the present study, C57BL/6 female mice (n=56) were used to explore the neuroprotective effects of riboflavin in motor disability of experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis.
Materials and Methods: The animals were assigned into 7 groups: sham-operated 1 (SO1), healthy mice receiving PBS (phosphate buffer saline); sham-operated 2 (SO2), healthy mice receiving PBS and riboflavin; sham treatment 1 (ST1), EAE mice receiving water; sham treatment 2 (ST2), EAE mice receiving sodium acetate buffer; treatment 1 (T1), EAE mice receiving interferon beta-1a (INFβ-1a); treatment 2 (T2), EAE mice receiving riboflavin; treatment 3 (T3), EAE mice receiving INFβ-1a and riboflavin. After EAE induction, scoring was performed based on clinical signs. Upon detecting score 0.5, riboflavin at 10 mg/kg of body weight and/or INFβ-1a at 150 IU/g of body weight administration was started for two weeks. The brain and spinal cord levels of brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), and interleukin-17A (IL-17A) were studied using real-time PCR and ELISA methods.
Results: BDNF expression and protein levels were increased in the brain and spinal cord of the T3 group compared with the other groups (P<0.01). IL-6 and IL-17A expressions were increased in the brains of the T3 and T1 groups, respectively, compared to the other groups (P<0.01). The daily clinical score was reduced significantly by riboflavin in both effector and chronic phases of the disease compared with that of the controls (P<0.05).
Conclusion: Our findings showed that riboflavin is capable of suppressing the neurological disability mediated by BDNF and IL-6.
https://ijbms.mums.ac.ir/article_6817_9a83199fd32878af97ce2388a2c1363c.pdf
2016-04-01
439
448
10.22038/ijbms.2016.6817
Brain-derived neurotrophic -factor
Experimental autoimmune -encephalomyelitis
Interleukin-17A
Interleukin-6
Motor disability
Riboflavin
Mahshid
Naghashpour
mnaghashpour@gmail.com
1
Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
AUTHOR
Reza
Amani
amani-r@ajums.ac.ir
2
Health Research Institute, Diabetes Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
AUTHOR
Alireza
Sarkaki
sarkaki145@gmail.com
3
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
LEAD_AUTHOR
Ata
Ghadiri
ata.ghadiri@hotmail.fr
4
Cell and Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
AUTHOR
Alireza
Samarbafzadeh
5
Infectious and Tropical Disease Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
AUTHOR
Sima
Jafarirad
6
Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
AUTHOR
Amal
Saki Malehi
amalsaki@gmail.com
7
Department of Vital Statistics, Faculty of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan, Iran
AUTHOR
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53
ORIGINAL_ARTICLE
Design of cocktail peptide vaccine against Cytomegalovirus infection
Objective(s):Human Cytomegalovirus (HCMV) remains a major morbidity and mortality cause in immuno suppressed patients. Therefore, significant effort has been made towards the development of a vaccine. In this study, the expression of the pp65 and gB fusion peptides and Fc domain of mouse IgG2a as a novel delivery system for selective uptake of antigens by antigen-presenting cells (APCs) in Pichia pastoris yeast system were studied.
Materials and Method: In this study, four immune dominant sequences in pp65 protein and 3 immuno dominant sequences in gB protein were selected according to literature review. Peptide linker -GGGGS- was used for construction of fusion peptide. This fusion peptide was cloned in the pPICZαA expression vector and transfected into P. pastoris host cells.
Results: Dot blot and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) techniques showed that a high level of pp65-gB-Fc fusion peptide was expressed.
Conclusion: This CMV pp65-gB-Fc fusion peptide could be a promising candidate for the development of a novel peptide vaccine.
https://ijbms.mums.ac.ir/article_6819_0b5ddae262f587de6498b818b339ef9d.pdf
2016-04-01
449
454
10.22038/ijbms.2016.6819
Human cytomegalovirus
pp65
Pichia pastoris
Peptide vaccine
Samira
Tabaei
samira.tabaee@gmail.com
1
Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
AUTHOR
Baratali
Mashkani
mashkaniba@mums.ac.ir
2
Department of Medical Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Arezoo
Esmaili
3
Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
AUTHOR
Reza
Karimi
reza.gene5@gmail.com
4
Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
AUTHOR
Saeid Amel
Jamehdar
meljs@mums.ac.ir
5
Antimicrobial Resistance Research Center, Avicenna Research Institute, Mashhad University of Medical Science, Mashhad, Iran
LEAD_AUTHOR
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15.Ahmad M, Hirz M, Pichler H, Schwab H. Protein expression in Pichia pastoris: recent achievements and perspectives for heterologous protein production. Appl Microbiol Biotechnol 2014; 98:5301–5317.
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infectious bursal disease virus VP2 in yeast. Iran J Vet Res 2013; 3:211-219.
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28