الفهرس | Only 14 pages are availabe for public view |
Abstract The present study aimed to investigate the possible nephro-and cardio-toxic effects of EGCG in diabetic mice. Moreover, this study explores the role of oxidative stress, inflammation, and apoptosis as possible mechanisms underlying EGCG toxicity. Streptozotocin (150 mg/kg, i.p.) was injected in mice for diabetes induction. EGCG (100 mg/kg/day, i.p.) was then given for 4 days. The administration of EGCG to diabetic mice caused 60% mortality with no death recorded in other groups. Blood samples were collected for estimation of renal biomarkers, such as serum cystatin C and neutrophil gelatinase-associated lipocalin in addition to myocardial biomarkers, such as creatine kinase-MB and troponin-I. Animals were then sacrificed, kidneys and hearts were rapidly excised for estimation of oxidative stress markers (NADPH oxidase, reduced glutathione, total antioxidant capacity, nuclear factor erythroid 2-related factor 2, heat shock protein 90, hemeoxygenase-1) as well as inflammatory markers (nuclear factor-kappa B and tumor necrosis factor-Ü). Administration of EGCG to diabetic mice showed significant elevation in renal and myocardial biomarkers, marked increase in oxidative stress and inflammatory states in addition to marked over expression of active caspase-3.Histopathological examination confirmed EGCG induced renal and myocardial damage in diabetic mice. In conclusion, despite of its well known favorable effects, EGCG could paradoxically exhibit nephro and cardio-toxic effects in the presence of diabetes |