Abstract
Numerous clinical and bioavailability studies addressed epigallocatechin gallate (EGCG) beneficial effects; however, our previous work revealed EGCG-induced nephrotoxicity in the presence of diabetes. In this study, the potential myocardial toxicity of EGCG preparation (100 mg/kg/day, IP; 4 days) in diabetic mice injected with streptozotocin (STZ; 150 mg/kg, IP) was investigated. Diabetic mice receiving EGCG preparation showed electrocardiographic changes in addition to elevation of both serum creatine kinase-MB and troponin-I levels accompanied by microscopic myocardial damage. Additionally, myocardial NADPH oxidase, lipid peroxides and nitrotyrosine were increased in the vicinity of decreases of nuclear factor erythroid 2-related factor 2, hemeoxygenase-1, reduced glutathione, total antioxidant capacity, glutathione peroxidase and reductase and heat shock protein 90. Moreover, in diabetic mice, EGCG preparation increased myocardial nuclear factor-kappa B and tumor necrosis factor-alpha in addition to pronounced overexpression of inducible nitric oxide synthase and active caspase-3. Therefore, this study substantiates that EGCG-mediated deterioration compromises diabetes-induced cardiotoxicity to solidify our previous report for its potential nephrotoxicity in the same experimental setting.
Highlights
Diabetes mellitus presents from a constellation of heterogeneous malfunctions witnessed by episodes of hyperglycemia and glucose intolerance resulting from lack and/or defective insulin or insulin action
EGCG group showed no alteration in these parameters compared to normal group
Administration of EGCG to diabetic mice markedly deteriorated these parameters compared to diabetic group confirming that EGCG preparation potentiated diabetes-induced myocardial damage (Table 1)
Summary
Diabetes mellitus presents from a constellation of heterogeneous malfunctions witnessed by episodes of hyperglycemia and glucose intolerance resulting from lack and/or defective insulin or insulin action This type of metabolic syndrome arises from derangements in the regulatory systems for storage and mobilization of metabolic fuels[1]. The administration of EGCG in the presence of lipopolysaccharide-induced fever or dyslipidemia in mice resulted in hepatotoxicity, while in colitic mice it induced nephrotoxicity[16,18]. Based on the data of our previous work signifying nephrotoxic effect of EGCG preparation in mice mediated by oxidative stress, inflammation and apoptosis, the current study was undertaken to delineate the potential car-
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