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Ameliorative effects of resveratrol against cadmium-induced nephrotoxicity via modulating nuclear xenobiotic receptor response and PINK1/Parkin-mediated Mitophagy.
Food & Function ( IF 5.1 ) Pub Date : 2020-02-18 , DOI: 10.1039/c9fo02287b
Qi Zhang 1 , Cong Zhang , Jing Ge , Mei-Wei Lv , Milton Talukder , Kai Guo , Yan-Hua Li , Jin-Long Li
Affiliation  

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.

中文翻译:

白藜芦醇通过调节核异源生物受体反应和PINK1 / Parkin介导的线粒体对镉诱导的肾毒性的改善作用。

镉是一种有毒污染物,在农业环境中具有很高的肾毒性。已经发现白藜芦醇具有肾脏保护作用,但是尚未完全阐明其潜在机制。这项研究的目的是说明白藜芦醇对镉诱导的肾毒性的拮抗作用。将总共​​80只家禽随机分为4组,并通过如下饮食90天进行处理:400 mg kg-1白藜芦醇组(Resv); 140 mg kg-1 Cd组(Cd 140); 140 mg kg-1 Cd + 400 mg kg-1白藜芦醇组(Cd + Resv)。观察到白藜芦醇治疗显着减轻了镉诱导的肾脏的组织病理学损害。同时,白藜芦醇通过减少MDA和H2O2的产生来减轻Cd诱导的氧化应激,减轻GSH消耗并恢复抗氧化酶(T-SOD,Cu-Zn SOD,CAT,GST和GSH-Px)的活性。白藜芦醇激活了NXR(CAR / PXR / AHR / Nrf2)信号通路,并通过增强I和II期排毒系统以减轻氧化损伤而发挥了解毒作用。此外,白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,改善了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。铜锌SOD,CAT,GST和GSH-Px)。白藜芦醇激活了NXR(CAR / PXR / AHR / Nrf2)信号通路,并通过增强I和II期排毒系统以减轻氧化损伤而发挥了解毒作用。此外,白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,改善了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。铜锌SOD,CAT,GST和GSH-Px)。白藜芦醇激活了NXR(CAR / PXR / AHR / Nrf2)信号通路,并通过增强I和II期排毒系统以减轻氧化损伤而发挥了解毒作用。此外,白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,改善了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。白藜芦醇激活了NXR(CAR / PXR / AHR / Nrf2)信号通路,并通过增强I和II期排毒系统以减轻氧化损伤而发挥了解毒作用。此外,白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,改善了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。白藜芦醇激活了NXR(CAR / PXR / AHR / Nrf2)信号通路,并通过增强I和II期排毒系统以减轻氧化损伤而发挥了解毒作用。此外,白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,改善了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,从而减轻了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。白藜芦醇通过恢复线粒体功能相关因子VDAC1,Cyt C和Sirt3上调以及Sirt1,PGC-1α,Nrf1和TFAM转录限制,从而减轻了镉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诱导的线粒体过度裂变,并促进了线粒体融合,从而逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。它逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。它逆转了PINK1 / Parkin介导的线粒体起始。总的来说,我们的发现阐明了针对Cd引起的肾毒性和线粒体损害的潜在保护作用。
更新日期:2020-02-26
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