Oxidative stress is a pathological state wherein oxidative forces surpass the antioxidant systems due to the loss of balance between them, leads to several diseased conditions including diabetes mellitus, atherosclerosis, hypertension, ischemic diseases and malignancies. Experimental and clinical studies evidenced that the chronic hyperglycemia in diabetes is associated with oxidative stress mediated tissue damage. Zinc is an essential trace element of exceptional biological and public health importance, especially in the prenatal and postnatal developments. Among the various tissues, pancreatic tissues are more susceptible to oxidative stress due to relatively less intrinsic antioxidant defense system. The present study was aimed to investigate the effect of zincdiosmin complex on hyperglycemia-mediated oxidative damage in pancreatic tissues of high fat diet fed -low dose streptozotocin induced experimental type 2 diabetes in rats. Diabetic rats were treated with zinc-diosmin complex (20 mg/kg b.w.) orally for 30 days. The extent of oxidative stress was assessed by determining the levels of lipid and hydroperoxides, pancreatic tissue antioxidants. In addition, the levels of pancreatic Nuclear factor (NF)-κB p65 unit, Nitric oxide (NO) in serum as well as pancreas and plasma TNF-α, IL-1β and IL-6 were determined. Zincdiosmin complex treatment to diabetic rats significantly improved the levels of antioxidants and reduced the levels of lipid peroxides and nuclear NF-κB p65 unit, NO levels in serum and pancreatic tissues. The levels of TNF-α, IL- 1β and IL-6 in plasma of diabetic rats were also reduced upon treatment with zinc-diosmin complex. Histological observations also clearly evidenced the pancreatic β-cell protective role of zinc-diosmin complex against hyperglycemia mediated oxidative damage which in turn attributed to the antioxidant potential of the complex.
