Volume 26, Issue 3 (Monthly-May 2015)                   Stud Med Sci 2015, 26(3): 252-259 | Back to browse issues page

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Microbiology Department, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran , n.delirezh@urmia.ac.ir
Abstract:   (4732 Views)

Background & Aims: It has been shown that some drugs such as Pentoxifylline (PTX) have immunomodulatory and anti-inflammatory activity that might represent a potential preventive therapy for autoimmune diseases. The purpose of this study was to investigate the therapeutic effects of pentoxifylline on the treatment of autoimmune diabetes in mice and its effects on expressions of peroxisome proliferator-activated receptor gamma (PPARγ) gene.

Materials & Methods: Diabetes was induced by multiple low-dose of streptozotocin (MLDS) injection (40 mg/kg/day for 5 consecutive days) in male C57BL/6 mice. After induction of diabetes, mice were treated with Pentoxifylline (100 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 cytokines production by ELISA. Subsequently expressions of peroxisome proliferator-activated receptor gamma (PPARγ) gene in spleens were tested by semi-quantitative RT-PC.

Results: Pentoxifylline treatment prevented hyperglycemia in the diabetic mice. Pentoxifylline treatment also significantly inhibited the production of proinflammatory cytokines interleukin 17 (IL-17) as well as interferon gamma (IFN-γ) while increased the level of anti-inflammatory cytokine IL-10 and upregulation of peroxisome proliferator-activated receptor gamma (PPARγ) gene expression in spleens as compared with those in diabetic control group (p< 0.05).

Conclusion: Finally, these findings indicate that Pentoxifylline 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 2015: 26(3): 259 ISSN: 1027-3727

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Type of Study: Research | Subject: آناتومی