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N-acetylcysteine attenuates PM2.5-induced apoptosis by ROS-mediated Nrf2 pathway in human embryonic stem cells  ( SCI-EXPANDED收录)   被引量:40

文献类型:期刊文献

英文题名:N-acetylcysteine attenuates PM2.5-induced apoptosis by ROS-mediated Nrf2 pathway in human embryonic stem cells

作者:Jin, Lifang[1];Ni, Jian[1];Tao, Yuan[1];Weng, Xinyi[1];Zhu, Yuling[1];Yan, Junyan[1];Hu, Baowei[1]

机构:[1]Shaoxing Univ, Sch Life Sci, Huancheng West Rd 508, Shaoxing 312000, Zhejiang, Peoples R China

年份:2019

卷号:666

起止页码:713

外文期刊名:SCIENCE OF THE TOTAL ENVIRONMENT

收录:SCI-EXPANDED(收录号:WOS:000463180700069)、、WOS

基金:This work has been generously supported by the Research Fund Program of National Natural Science Foundation of China (No. 21876115), as well the scientific research start-up funding of Shaoxing University (Grant No. 20185009).

语种:英文

外文关键词:PM2.5; Human embryonic stem cells; Apoptosis; Oxidative stress; Nrf2 pathway; N-acetylcysteine

外文摘要:While the effects of fine particulate matter (PM2.5) on embryonic toxicity are widely accepted, its exact mechanisms have not yet been fully elucidated, which partially attribute to lack of ideal research model. Embryonic stem cells (ESCs) have the capacity to differentiate into all cell types of three germ layers. Thus, they are ideal resources for the reproductive toxicity assessment. in vitro. In the present study, we investigated the effects of PM2.5 exposure on the oxidative stress and apoptosis of human ESCs (hESCs) and its possible mechanism. Our results showed that strong cytotoxicity high reactive oxygen species (ROS) level and fragmentation of nuclei were observed in the PM2.5-treated hESCs. Meanwhile, up-regulation of apoptosis as well as down regulation of Nrf2 signaling pathway were also observed after PM2.5 treatment. However, we did not detect. significant. expression change or phosphorylation of Akt and Erk in PM2.5-treated hESCs. Interestingly, scavenging of PM2.5-induced ROS by N-acetylcysteine (NAC) could block cell apoptosis and rescue the activity of Nrf2 signaling pathway. In conclusion, we demonstrate that PM2.5 is toxic to hESCs by inhibition of ROS-mediated Nrf2 pathway activity. Our findings suggest activation of Nrf2 pathway will help develop new strategies for the prevention and treatment of PM2.5-associated disease. (C) 2019 Elsevier B.V. All rights reserved.

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