E J Chang1, K C Mun. 1. Dong San Kidney Institute and Chronic Disease Research Center, Keimyung University School of Medicine, Daegu, Korea.
Abstract
INTRODUCTION: Nephrotoxicity is a clinically important side effect of cyclosporine (CsA). CsA-induced nephrotoxicity results from increased production of free radical species in the kidney. Epigallocatechin gallate (EGCG) acts as an antioxidant, thus, EGCG may have a protective effect on the alteration of renal function resultant from oxygen free radicals. The purpose of the present study was to investigate the protective effect of EGCG in a rodent model. METHODS: Experiments were performed on 3 groups. The normal control group (group 1) received normal saline solution. The CsA-treated group (group 2; 15 mg/kg body weight/d for 14 days) received subcutaneous injections. The EGCG-treated group (group 3) in addition received 25 mg of EGCG/kg body weight by intraperitoneal injection. RESULTS: There were significant increases in levels of blood urea nitrogen (BUN)(42.8 +/- 8.2 mg/dL; P < .001), serum creatinine (1.18 +/- 0.60 mg/dL; P < .05), and serum malondialdehyde (3.09 +/- 0.20 nmol/mL; P < .001), and a significant decrease in CCr(0.07 +/- 0.02 mL/min; P < .001) in group 2 compared with group 1. Levels of BUN (30.2 +/- 0.7 mg/dL; P < .01)and CCr (0.12 +/- 0.08 mL/min) were lower in group 3 than in group 2. Serum creatinine (0.71 +/- 0.04 mg/dL) and serum malondialdehyde level (2.13 +/- 0.15; P < .001 nmol/mL) were lower in group 3 than in group 2. There was no significant difference in CsA levels between group 2 (6.86 +/- 1.48 mug/mL) and group 3 (6.69 +/- 0.62 mug/mL). CONCLUSIONS: EGCG treatment significantly protected renal function and free radical-mediated injury in the kidney from CsA-induced changes.
INTRODUCTION:Nephrotoxicity is a clinically important side effect of cyclosporine (CsA). CsA-induced nephrotoxicity results from increased production of free radical species in the kidney. Epigallocatechin gallate (EGCG) acts as an antioxidant, thus, EGCG may have a protective effect on the alteration of renal function resultant from oxygen free radicals. The purpose of the present study was to investigate the protective effect of EGCG in a rodent model. METHODS: Experiments were performed on 3 groups. The normal control group (group 1) received normal saline solution. The CsA-treated group (group 2; 15 mg/kg body weight/d for 14 days) received subcutaneous injections. The EGCG-treated group (group 3) in addition received 25 mg of EGCG/kg body weight by intraperitoneal injection. RESULTS: There were significant increases in levels of blood ureanitrogen (BUN)(42.8 +/- 8.2 mg/dL; P < .001), serum creatinine (1.18 +/- 0.60 mg/dL; P < .05), and serum malondialdehyde (3.09 +/- 0.20 nmol/mL; P < .001), and a significant decrease in CCr(0.07 +/- 0.02 mL/min; P < .001) in group 2 compared with group 1. Levels of BUN (30.2 +/- 0.7 mg/dL; P < .01)and CCr (0.12 +/- 0.08 mL/min) were lower in group 3 than in group 2. Serum creatinine (0.71 +/- 0.04 mg/dL) and serum malondialdehyde level (2.13 +/- 0.15; P < .001 nmol/mL) were lower in group 3 than in group 2. There was no significant difference in CsA levels between group 2 (6.86 +/- 1.48 mug/mL) and group 3 (6.69 +/- 0.62 mug/mL). CONCLUSIONS:EGCG treatment significantly protected renal function and free radical-mediated injury in the kidney from CsA-induced changes.