| Background:Cisplatin (CP) is a commonly used anticancer drug, but its notable side effect of nephrotoxicity limits its use in clinic. Epigallocatechin-3-gallate (EGCG), an anti-oxidant, anti-inflammatory, and anti-tumorigenic green tea polyphenol, has been available on the market for its beneficial effects.Aim:The aim of this study was to investigate whether EGCG can prevent the nephrotoxic effect of CP and the involved mechanisms.Methods:A total of 28 male C57/BL6 mice were divided randomly in the following five groups:(1) control group (NC; n=7), only received intraperitoneal (i.p.) injection of vehicle solution (0.9% saline; 10 ml/kg); (2) EGCG group (EGCG; n=7), received a single i.p. injection of 100 mg/kg EGCG (dissolved in 0.9% saline to reach 20 mg/ml); (3) CP group (CP; n=7), only received an i.p. injection of 20.0 mg/kg CP (dissolved in 0.9% saline to reach a concentration of 2.0 mg/ml); and (4) CP+EGCG 100 mg/kg group (CP+EGCG 100 mg/kg; n= 7), which successively received i.p. injection of 100 mg/kg EGCG at 30 min before i.p. injection of CP, and i.p. administration of 100 mg/kg EGCG after i.p. injection of CP 48 h.5 days after i.p. injection of CP, all mice were sacrificed by cervical dislocation, and all of them were weighed and blood was collected from the endocanthion before the sacrifice.Results:Our results showed that EGCG treatment significantly ameliorated the histopathological changes and the increased serum creatinine and blood urea nitrogen (BUN) induced by CP. TUNEL-positive cells significantly reduced in the CP+EGCG group compared with CP group. EGCG also inhibited the expression of the ligand of death receptor Fas (Fas-L), apoptosis regulator BAX (Bax) and tumor-suppressor protein p53, and increased the expression of B-cell lymphoma 2 (Bcl-2). These findings suggest that EGCG can ameliorate CP-induced apoptosis in the kidney by regulating death receptor Fas conducted extrinsic pathway, and the expression of Bax and Bcl-2. |
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