APIGENIN CAUSES BIOCHEMICAL MODULATION, GLUT4 AND CD38 ALTERATIONS TO IMPROVE DIABETES AND TO PROTECT DAMAGES OF SOME VITAL ORGANS IN EXPERIMENTAL DIABETES

Abstract

Diabetes mellitus gradually leads to dysfunction an d failure of some vital organs specially the eyes, kidneys, pancreas, brain, heart, liver and lungs. The study was aimed to evaluate the antidiabetic potential of apigenin and its mechanistic role in controlling damages of vital tissues in streptozotocin-induced diabetic ra ts. Streptozotocin-induced diabetic rats were treated w ith apigenin and glipizide. Various biochemical cha nges, GLUT4 and CD38 protein expression patterns and histopathological alterations in some vital organs such as liver, kidneys and pancreas were investigated to co mpare the antidiabetic potentials of those two chem icals and to understand their capability to control the d amages of the vital organs during diabetes. Effecti ve control of blood glucose level along with the alteration of hepatic phase I and phase II drug metabolizing enz ymes, antioxidant defense enzyme activities and lipid per oxidation level towards their normal values and enh anced GLUT4 translocation and downregulated CD38 expression by apigenin were observed. Apigenin was also found to prevent the deterioration of vital organs during diabetes. In conclusion, apigenin has predom inant role in controlling blood glucose level along with the p rotection of vital organs eventually damaged during diabetes, by minimizing toxicities and associated d iabetic complications in streptozotocin-induced dia betic rats and may explore as a potential antidiabetic agent i n near future.