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Methoxy VO–salen Stimulates Pancreatic β Cell Survival by Upregulation of eNOS and Downregulation of Apoptosis in STZ-induced Diabetic Rats

Author:
Roy, Souvik, Mondru, Anil Kumar, Dontamalla, Sudheer Kumar, Vaddepalli, Ram Prasad, Sannigrahi, Santanu, Veerareddy, Prabhakar Reddy
Source:
Biological trace element research 2011 v.144 no.1-3 pp. 1095-1111
ISSN:
0163-4984
Subject:
antioxidants, apoptosis, blood glucose, blood serum, catalase, cell viability, cholesterol, diabetes, glutathione, high density lipoprotein, histopathology, immunohistochemistry, lipid peroxidation, nitric oxide synthase, oxidative stress, pancreas, rats, streptozotocin, superoxide dismutase, toxicity, triacylglycerols
Abstract:
The present study was designed to investigate the effect of MetVO–salen in ameliorating diabetes and oxidative stress in the pancreas of diabetic rats. Streptozotocin (STZ)-induced diabetic rats were treated with MetVO–salen complex intraperitonially (0.3 and 0.6 mg/kg) thrice a week and continued for 8 weeks. Total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides in serum, and blood glucose were estimated. Furthermore, oxidative stress in rats was also investigated in terms of superoxide dismutase (SOD), catalase, lipid peroxidation, and glutathione (GSH). In addition, the anti-diabetic activity of MetVO–salen was also investigated by assessing histopathological, immunohistochemical in terms of endothelial nitric oxide synthase expression, and apoptotic events in pancreas. Treatment with MetVO–salen complex reduced the blood glucose level and significantly altered the serum biochemical parameters of diabetic rats. Treatment with above complex decreased the lipid peroxidation and the antioxidant enzymes such as SOD, CAT, and GSH to near-control levels. Histopathological, immunohistochemical, and apoptotic studies also revealed that MetVO–salen-induced amelioration of the diabetic state appears to be significant to the preservation of a functional portion of the pancreatic β cells which initially prevent STZ toxicity. This study provides new direction for the management of diabetes but needs further clinical evaluation.
Agid:
150613