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白藜芦醇通过调节核异源生物受体反应和 PINK1/Parkin 介导的线粒体自噬来减轻镉诱导的肾毒性。

Ameliorative effects of resveratrol against cadmium-induced nephrotoxicity via modulating nuclear xenobiotic receptor response and PINK1/Parkin-mediated Mitophagy.

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, P. R. China.

出版信息

Food Funct. 2020 Feb 26;11(2):1856-1868. doi: 10.1039/c9fo02287b.

Abstract

Cadmium (Cd) is a toxic pollutant with high nephrotoxicity in the agricultural environment. Resveratrol has been found to have a renoprotective effect but the underlying mechanisms of this have not yet been fully elucidated. The aim of this study is to illustrate the antagonism of resveratrol against Cd-induced nephrotoxicity. A total of 80 birds were divided randomly into 4 groups and treated via diet for 90 days as follows: control group (Con); 400 mg kg-1 resveratrol group (Resv); 140 mg kg-1 Cd group (Cd 140); and 140 mg kg-1 Cd + 400 mg kg-1 resveratrol group (Cd + Resv). It was observed that resveratrol treatment dramatically alleviated Cd-induced histopathological lesions of the kidney. Simultaneously, resveratrol mitigated Cd-induced oxidative stress by reducing MDA and H2O2 production, alleviating GSH depletion and restoring the activity of antioxidant enzymes (T-SOD, Cu-Zn SOD, CAT, GST and GSH-Px). Resveratrol activated NXRs (CAR/PXR/AHR/Nrf2) signaling pathways and exerted antidotal roles by enhancing the phase I and II detoxification systems to relieve oxidative damage. Moreover, resveratrol ameliorated Cd-induced ultrastructural abnormality and mitochondria dysfunction by recovering mitochondrial function-related factors VDAC1, Cyt C and Sirt3 upregulation and Sirt1, PGC-1α, Nrf1 and TFAM transcription restrictions. Resveratrol attenuated Cd-induced excessive mitochondrial fission and promoted mitochondrial fusion, which reversed PINK1/Parkin-mediated mitophagy initiation. Collectively, our findings explicate the potential protection against Cd-induced nephrotoxicity and mitochondria damage.

摘要

镉(Cd)是农业环境中具有高肾毒性的有毒污染物。白藜芦醇已被发现具有肾保护作用,但这一作用的潜在机制尚未完全阐明。本研究旨在阐明白藜芦醇对镉诱导的肾毒性的拮抗作用。共 80 只鸟类随机分为 4 组,通过饮食处理 90 天,如下所示:对照组(Con);400mgkg-1白藜芦醇组(Resv);140mgkg-1Cd 组(Cd140);和 140mgkg-1Cd+400mgkg-1白藜芦醇组(Cd+Resv)。结果表明,白藜芦醇处理显著减轻了 Cd 诱导的肾脏组织病理学损伤。同时,白藜芦醇通过减少 MDA 和 H2O2 的产生,减轻 GSH 耗竭,恢复抗氧化酶(T-SOD、Cu-Zn SOD、CAT、GST 和 GSH-Px)的活性,减轻 Cd 诱导的氧化应激。白藜芦醇激活了 NXRs(CAR/PXR/AHR/Nrf2)信号通路,并通过增强 I 相和 II 相解毒系统发挥解毒作用,从而减轻氧化损伤。此外,白藜芦醇通过恢复与线粒体功能相关的因子 VDAC1、Cyt C 和 Sirt3 的上调以及 Sirt1、PGC-1α、Nrf1 和 TFAM 转录限制,改善了 Cd 诱导的超微结构异常和线粒体功能障碍。白藜芦醇减轻了 Cd 诱导的线粒体过度分裂,并促进了线粒体融合,从而逆转了 PINK1/Parkin 介导的线粒体自噬起始。总之,我们的研究结果阐明了白藜芦醇对 Cd 诱导的肾毒性和线粒体损伤的潜在保护作用。

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