期刊
FOOD AND CHEMICAL TOXICOLOGY
卷 96, 期 -, 页码 70-78出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2016.07.030
关键词
Cadmium; Epigallocatechin-3-gallate; Renal injury; Oxidative stress; Transforming growth factor-beta 1
资金
- Youth Science and Technology Plan of Wuhan, China [2015071704011629]
- Natural Science Fund of Hubei Province, China [2015CFB250]
Cadmium (Cd)-pollution is a serious environmental problem. Kidney is a main target organ of Cd toxicity. This study was undertaken to investigate the potential protective effects of epigallocatechin-3-gallate (EGCG) against chronic renal injury and fibrosis induced by CdCl2. Rat model was induced by exposing to 250 mg/L CdCl2 through drinking water. The renal function was evaluated by detecting the levels of blood urea nitrogen (BUN) and serum creatinine (SCR). The oxidative stress was measured by detecting the levels of malondialdehyde (MDA), nitric oxide (NO), reduced glutathione/oxidized glutathione (GSH/GSSG) and renal enzymatic antioxidant status. Additionally, the renal levels,of transforming growth factor-beta 1 (TGF-beta 1), Smad3, phosphorylation-Smad3 (pp-Smad3), alpha-smooth muscle actin (alpha-SMA), vimentin and E-cadherin were measured by western blot assay. Renal levels of microRNA-21 (miR-21), miR-29a/b/c and miR-192 were measured by quantitative RT-PCR. It was found that EGCG ameliorated the CdCl2-induced renal injury, inhibited the level of oxidative stress, normalized renal enzymatic antioxidant status and E-cadherin level, as well as attenuated the over generation of TGF-beta 1, pp-Smad3, vimentin and alpha-SMA. EGCG also decreased the production of miR-21 and miR-192, and enhanced the levels of miR-29a/b/c. These results showed that EGCG could attenuate Cd induced chronic renal injury. (C) 2016 Elsevier Ltd. All rights resenied.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据