Protective effect of EGCG on renal ischemia-reperfusion injury

Objective To explore the protective effects of EGCG on renal ischemia-reperfusion injury( IRI) and the mechanism. Methods Male SD rats were randomly divided into Sham,IRI and EGCG( low,middle and high dose) groups. The model of IRI was induced by clamping the bilateralrenal pedicles for 45 min and r...

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Bibliographic Details
Main Authors: ZUO Song, ZHANG Jiong
Format: Article
Language:zho
Published: Editorial Department of Journal of Clinical Nephrology 2017-01-01
Series:Linchuang shenzangbing zazhi
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Online Access:http://www.lcszb.com/thesisDetails?columnId=57917541&Fpath=home&index=0
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Summary:Objective To explore the protective effects of EGCG on renal ischemia-reperfusion injury( IRI) and the mechanism. Methods Male SD rats were randomly divided into Sham,IRI and EGCG( low,middle and high dose) groups. The model of IRI was induced by clamping the bilateralrenal pedicles for 45 min and removing right kidney,successive reperfusion for 24 h. The levels of SCr,BUN,IFN-γ,TNF-αand IL-6 in the serum were examined by ELISA. The expression levels of Wnt,β-catenin,p53 and p21 were detected by Western blotting. The expression of MDA was measured by TBA. Moreover,the morphrologic changes of kidney and the activation of CAT,GPX and SOD in the kidney were measured by PAS and hydrogen peroxide enzyme,respectively. Results Compared to Sham group,the levels of SCr,BUN,IFN-γ,TNF-α,IL-6,Wnt,β-catenin,p53,p21 and MDA were significantly increased,the pathological changes of the kidney significantly aggravated and activities of CAT,GPx and SOD significantly reduced in the kidney in the IRI group. Compared to IRI group,the levels of SCr,BUN,IFN-γ,TNF-α,IL-6,Wnt,β-catenin,p53,p21 and MDA were significantly reduced,pathological changes of the kidney alleviated and activities of CAT,GPXand SOD in the kidney increased in the EGCG group. Conclusions EGCG preconditioning can reduce kidney IRI by suppressing inflammation and oxidative stress in rats,which may be associated with the inhibition of Wnt/β-catenin/p53 signal pathway activation.
ISSN:1671-2390