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Epigallocatechin gallate attenuate Cisplatin induced acute renal failure in rat

Abstract
Cisplatin is one of the most effective chemotherapeutic agents used in treatment of a variety of human solid tumors. The most common adverse side effect limiting the use of Cisplatin is nephrotoxicity. Recent studies indicate that inflammatory and oxidative signaling play critical role in pathogenesis of Cisplatin related nephrotoxicity. Cisplatin-induced nephrotoxicity is associated with lipid peroxidation and the superoxide anion and hydroxyl radical scavenger could prevent acute renal failure through both attenuation of tubular damage and enhanced regenerative response of the damaged tubular cells. It has been shown that green tea polyphenols with antioxidant properties inhibit inflammatory and oxidative responses in mice. However, the evidence indicating the protective effect of epigallocatechin gallate (EGCG), the major polyphenol found in green tea, on Cisplatin-induced nephrotoxicity is lacking. The present study is to evaluate the effect of EGCG injection on Cisplatin-induced nephrotoxicity in rats. The male rats were divided into four groups (n = 6 each); control group, Cisplatin group, EGCG group and Cisplatin + EGCG group. The control group received only intraperitoneal normal saline injection. Cisplatin (6 mg/kg) was given single dose intraperitoneally at day 0, EGCG (10 mg/time) was given subcutaneously at day 4, day 2 and day 0 before Cisplatin challenge and day 2 and day 4 after Cisplatin injection. Nephrotoxicity was evaluated by biochemical analysis of blood and histopathological observations of rat kidney. Nuclear factor-kappa B (NF-£eB) activation, inducible nitric oxide synthase (iNOS) expression and malonyldialdehyde (MDA) content were also determined in rat kidney. Cisplatin injection induced an increase in serum blood urea nitrogen, creatinine and tubular necrosis, and upregulation of NF-£eB and iNOS expression and MDA content in kidney. All the increases were significantly inhibited by EGCG treatment. The results suggest that EGCG may attenuate Cisplatin induced nephrotoxicity through the anti-inflammatory/oxidative effects.

Identiferoai:union.ndltd.org:NSYSU/oai:NSYSU:etd-0819110-105433
Date19 August 2010
CreatorsLiu, Ye-Chong
ContributorsChen, Hsien-Jung, Hsu, Ching-Mei, Liu, Jong-Kang
PublisherNSYSU
Source SetsNSYSU Electronic Thesis and Dissertation Archive
LanguageCholon
Detected LanguageEnglish
Typetext
Formatapplication/pdf
Sourcehttp://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0819110-105433
Rightsoff_campus_withheld, Copyright information available at source archive

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