Role of autophagy and oxidative stress to astrocytes in fenpropathrin-induced Parkinson-like damage

被引:13
|
作者
Wu, Yixuan [1 ,2 ,3 ,4 ]
Jiao, Zhigang [1 ,2 ,3 ,4 ]
Wan, Zhiting [1 ,2 ,3 ]
Qu, Shaogang [1 ,2 ,3 ]
机构
[1] Southern Med Univ, Dept Neurol, Nanfang Hosp, Guangzhou 510515, Guangdong, Peoples R China
[2] Guangdong Hong Kong Macao Greater Bay Area Ctr Br, Guangzhou 510515, Guangdong, Peoples R China
[3] Southern Med Univ, Minist Educ, Key Lab Mental Hlth, Guangzhou 510515, Guangdong, Peoples R China
[4] Southern Med Univ, Sch Basic Med Sci, Guangzhou 510515, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Fenpropathrin; Astrocytes; Oxidative stress; Autophagy; GLUTAMATE TRANSPORTER; IMPAIRED AUTOPHAGY; MOUSE MODEL; TIME-COURSE; DISEASE; PHOSPHORYLATION; CONTRIBUTES; ACTIVATION; INHIBITION; EXPRESSION;
D O I
10.1016/j.neuint.2021.105000
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Fenpropathrin is an insecticide that is widely used in agriculture. It remains unknown whether fenpropathrin exposure increases the risk of Parkinson?s disease. We found that fenpropathrin increased oxidative stress both in vitro and in vivo. Additionally, fenpropathrin increased production of ROS, NOS2, and HO-1, and decreased SOD and GSH in astrocytes. We further found that fenpropathrin-mediated oxidative stress might inhibit autophagic flow, including decreased expression of LC3A/B and enhanced expression of SQSTM1 via down-regulation of CDK-5, an upstream marker of autophagy. In mice, autophagy was slightly different from that found in astrocytes, as reflected in the increased expressions of LC3A/B and SQSTM1. Our findings elucidate the toxicological phenomena and pathogenic mechanisms of fenpropathrin and may provide guidance for improved pesticide control and environmental protection.
引用
收藏
页数:13
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