Volume 25, Issue 9 (Monthly Nov 2014)                   J Urmia Univ Med Sci 2014, 25(9): 784-790 | Back to browse issues page

XML Persian Abstract Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Malekifard F, Delirezh N, Hobbenaghi R, Malekinejad H. TREATMENT OF TYPE I DIABETIC MICE WITH AL-TRANS RETINOIC ACID BY INHIBITION OF PROINFLAMMATORY CYTOKINES. J Urmia Univ Med Sci. 2014; 25 (9) :784-790
URL: http://umj.umsu.ac.ir/article-1-2488-en.html
Department of Microbiology, School of Veterinary Medicine, Urmia University , n.delirezh@urmia.ac
Abstract:   (3632 Views)

  

  Background & Aims: Type 1 diabetes is an autoimmune condition associated with the T-cell–mediated destruction of Pancreatic β cells. Vitamin A (retinol) and its metabolites (such as all-trans retinoic acid (ATRA)) have a variety of biological activities including immunomodulatory action in a number of inflammatory and autoimmune conditions. The purpose of this study was to investigate the effects of all-trans retinoic acid on the treatment of autoimmune diabetes in mice.

 Materials & Methods: Diabetes was induced by multiple low-dose of streptozotocin (MLDS) injection in male C57BL/6 mice. After induction of diabetes, mice were treated with ATRA (20 mg/kg/day i.p.) for 21 days. Blood glucose levels was measured in 0, 7, 14 and 21 days after Streptozotocin induction induced diabetes. Splenocytes were tested for proliferation by MTT test and cytokine production by ELISA.

 Results: ATRA treatment prevented hyperglycemia in the diabetic mice. Aside from reducing lymphocyte proliferation, ATRA significantly inhibited the production of proinflammatory cytokines interleukin 17 (IL-17) as well as interferon gamma (IFN-γ) while it increased the level of anti-inflammatory cytokines IL-10 and TGF-β compared with those in diabetic control group (p<0.05).

 Conclusion: Treatment with ATRA in the diabetic mice prevented hyperglycemia, decreased lymphocyte proliferation, and inhibited the production of proinflammatory cytokines interleukin 17 (IL-17) as well as interferon gamma (IFN-γ). In addition, it increased anti-inflammatory cytokines IL-10 and TGF-β as compared with those in diabetic control group. These findings indicate that ATRA may have a therapeutic effect against the autoimmune destruction of the pancreatic beta-cells during the development of MLDS-induced type 1 diabetes in mice.

 

 SOURCE: URMIA MED J 2014: 25(9): 790 ISSN: 1027-3727

Full-Text [PDF 430 kb]   (768 Downloads)    
Type of Study: Research | Subject: آناتومی

Add your comments about this article : Your username or Email:
CAPTCHA code

Send email to the article author


© 2018 All Rights Reserved | URMIA MEDICAL JOURNAL

Designed & Developed by : Yektaweb