Epigallocatechin‐3‐gallate protects kidneys from ischemia reperfusion injury by HO‐1 upregulation and inhibition of macrophage infiltration

Summary Epigallocatechin‐3‐gallate (EGCG) shows diverse chemical and biological activities. We investigated the effects of EGCG in a rat renal ischemia reperfusion (I/R) injury model. Sprague–Dawley rats received intraperitoneal injection of 50 mg/kg EGCG 48 h, 24 h, and 30 min prior to I/R injury. The animals were subjected to left renal occlusion for 45 min. EGCG treatment suppressed the peak in serum creatinine. EGCG‐treated kidneys showed significantly less tubular damage and a decreased number of apoptotic cells. The I/R‐induced elevation in the renal MDA level was significantly decreased in the EGCG group. Reverse‐transcriptase polymerase chain reaction showed that EGCG significantly decreased the expression of MHC class II, TLR2, TLR4, MCP‐1, IL‐18, TGF‐β1, procollagen Ia1, TIMP‐1, and Kim‐1. ED‐1 staining showed reduced macrophage infiltration and α‐SMA staining revealed less interstitial expression. Heme oxygenase‐1 (HO‐1) expression in I/R kidneys was upregulated in the EGCG group based on the results of both RT‐PCR and Western blotting analysis. Blockade of HO‐1 gene induction by SnPP increased renal tubular damage and macrophage infiltration. These findings suggest that EGCG protects the kidneys against I/R injury by reducing macrophage infiltration and decreasing renal fibrosis. These beneficial effects may be mediated, in part, by augmentation of the HO‐1 gene.