@article {10.3844/ajptsp.2014.39.52, article_type = {journal}, title = {APIGENIN CAUSES BIOCHEMICAL MODULATION, GLUT4 AND CD38 ALTERATIONS TO IMPROVE DIABETES AND TO PROTECT DAMAGES OF SOME VITAL ORGANS IN EXPERIMENTAL DIABETES}, author = {Hossain, Chowdhury Mobaswar and Ghosh, Miltu Kumar and Satapathy, Bhabani Sankar and Dey, Niladri Shekhar and Mukherjee, Biswajit}, volume = {9}, year = {2014}, month = {Jan}, pages = {39-52}, doi = {10.3844/ajptsp.2014.39.52}, url = {https://thescipub.com/abstract/ajptsp.2014.39.52}, abstract = {Diabetes mellitus gradually leads to dysfunction and 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 rats. Streptozotocin-induced diabetic rats were treated with apigenin and glipizide. Various biochemical changes, GLUT4 and CD38 protein expression patterns and histopathological alterations in some vital organs such as liver, kidneys and pancreas were investigated to compare the antidiabetic potentials of those two chemicals and to understand their capability to control the damages of the vital organs during diabetes. Effective control of blood glucose level along with the alteration of hepatic phase I and phase II drug metabolizing enzymes, antioxidant defense enzyme activities and lipid peroxidation level towards their normal values and enhanced 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 predominant role in controlling blood glucose level along with the protection of vital organs eventually damaged during diabetes, by minimizing toxicities and associated diabetic complications in streptozotocin-induced diabetic rats and may explore as a potential antidiabetic agent in near future.}, journal = {American Journal of Pharmacology and Toxicology}, publisher = {Science Publications} }