Chen Jinglou, Du Lifen, Li Jingjing, Song Hongping
Department of Pharmacy, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Pharmacy, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Food Chem Toxicol. 2016 Oct;96:70-8. doi: 10.1016/j.fct.2016.07.030. Epub 2016 Jul 27.
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-β1 (TGF-β1), Smad3, phosphorylation-Smad3 (pp-Smad3), α-smooth muscle actin (α-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-β1, pp-Smad3, vimentin and α-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.
镉（Cd）污染是一个严重的环境问题。肾脏是镉毒性的主要靶器官。本研究旨在探讨表没食子儿茶素-3-没食子酸酯（EGCG）对氯化镉（CdCl2）诱导的慢性肾损伤和纤维化的潜在保护作用。通过饮用水中添加250 mg/L CdCl2诱导大鼠模型。通过检测血尿素氮（BUN）和血清肌酐（SCR）水平评估肾功能。通过检测丙二醛（MDA）、一氧化氮（NO）、还原型谷胱甘肽/氧化型谷胱甘肽（GSH/GSSG）水平和肾脏酶抗氧化状态来测定氧化应激。此外，通过蛋白质印迹法检测肾脏中转化生长因子-β1（TGF-β1）、Smad3、磷酸化-Smad3（pp-Smad3）、α-平滑肌肌动蛋白（α-SMA）、波形蛋白和E-钙黏蛋白的水平。通过定量逆转录聚合酶链反应（qRT-PCR）检测肾脏中微小RNA-21（miR-21）、miR-29a/b/c和miR-192的水平。结果发现，EGCG改善了CdCl2诱导的肾损伤，抑制了氧化应激水平，使肾脏酶抗氧化状态和E-钙黏蛋白水平恢复正常，同时减轻了TGF-β1、pp-Smad3、波形蛋白和α-SMA的过度生成。EGCG还降低了miR-21和miR-192的产生，并提高了miR-29a/b/c的水平。这些结果表明，EGCG可以减轻镉诱导的慢性肾损伤。
