粒体自噬
上睑下垂
帕金
炎症体
线粒体ROS
细胞生物学
活性氧
品脱1
化学
线粒体
程序性细胞死亡
氧化应激
细胞凋亡
自噬
生物化学
生物
医学
受体
病理
疾病
帕金森病
作者
Lei Tian,Ning Li,Kang Li,Yizhe Tan,Jie Han,Bencheng Lin,Wenqing Lai,Huanliang Liu,Yue Shi,Zhuge Xi,Xiaohua Liu
标识
DOI:10.1016/j.ecoenv.2022.113663
摘要
To study the regulatory relationship between ozone-induced mitophagy and pyroptosis in lung epithelial cells.First, type I primary alveolar epithelial cells and male Wistar rats were treated with ozone at different dosages. The ATP content and mitochondrial membrane potential significantly decreased in type I primary alveolar epithelial cells. The mitophagy-related markers and PINK1/Parkin pathway-related proteins, and the co-localization of LC3, Parkin, and mitochondria in type I alveolar epithelial cells indicated that ozone exposure triggered mitophagy. On the other hand, the reactive oxygen species (ROS) inhibitor NAC could significantly alleviate mitophagy in epithelial cells. After treatment with the mitophagy inhibitor MDIVI-1, the levels of the NLRP3 inflammasome, cleaved caspase-1, and N-gasdermin D (N-GSDMD) significantly decreased in the cells. Altogether, these results indicated that mitophagy can be triggered by ozone exposure, and subsequently induces cell death mediated by the NLRP3 inflammasome. Finally, the overexpression and knockdown of NLRP3 confirmed this conclusion.Ozone exposure induced oxidative damage, leading to mitochondrial structural and functional damage. Ozone-induced ROS triggered mitophagy through the activation of the PINK1/Parkin signaling pathway, then pyroptosis through activation of the NLRP3 inflammasome.
科研通智能强力驱动
Strongly Powered by AbleSci AI