TREATMENT OF TYPE I DIABETIC MICE WITH AL-TRANS RETINOIC ACID BY INHIBITION OF PROINFLAMMATORY CYTOKINES

Malekifard, F and Malekinejad, H and Hobbenaghi, R and Delirezh, N (2014) TREATMENT OF TYPE I DIABETIC MICE WITH AL-TRANS RETINOIC ACID BY INHIBITION OF PROINFLAMMATORY CYTOKINES. The Journal of Urmia University of Medical Sciences, 25 (9). p. 784.

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Abstract

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 antiinflammatory 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

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