Influence of gallic acid on oxidative stress-linked streptozotocin-induced pancreatic dysfunction in diabetic rats

Abstract

Recent advances in diabetic research involve the evaluation of agents that can regenerate or reverse pancreatic dysfunction. Although gallic acid (GA) has been reported as an antidiabetic agent, its ability to directly reverse altered biochemical parameters in diabetic pancreas has not been demonstrated. Male albino rats with diabetes induced by the administration of streptozotocin (STZ) (50 mg/kg, intraperitoneally) were treated with oral administration of GA. Antioxidants (enzymatic and non-enzymatic), purinergic enzymes, δ-aminolevulinic acid dehydratase and lactate dehydrogenase were evaluated in the pancreas of both diabetic and nondiabetic animals. The pharmacological effect of GA was accompanied by a restoration of the observed decreased levels of vitamin C and reduced glutathione in the pancreas of STZ-treated rats. GA also caused a marked reduction in the high levels of thiobarbituric acid reactive substances observed in the STZ-induced diabetic group. Furthermore, GA also improves the free radical scavenging property, Fe2+ chelating ability and Fe3+ reducing property of the pancreas of diabetic animals. Finally, the inhibition of pancreatic catalase, glutathione S-transferase, δ-aminolevulinic acid dehydratase and lactate dehydrogenase and increased activity of purinergic enzymes accompanied by hyperglycemia were prevented by GA in the pancreas. The direct influence and consequent restoration of altered biochemical conditions in the pancreatic tissue of diabetic animal models by GA makes it a promising antidiabetic candidate especially in pancreatic cell regeneration.