中国医科大学学报2019，Vol.48Issue(1)：1-6,6.DOI:10.12007/j.issn.0258-4646.2019.01.001
MnTMPyP通过抑制氧化应激和内质网应激减轻百草枯致肺上皮细胞损伤
MnTMPyP Reduces Paraquat-Induced Lung Epithelial-Like Cell Injury by Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress
摘要
Abstract
Objective To investigate the protective effect and underlying mechanism of the superoxide dismutase mimic, manganese (Ⅲ) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP), on paraquat (PQ) -induced lung epithelial-like cell injury. Methods Alveolar epithelial-like cells (A549) were pretreated with 10 μmol/L of MnTMPyP for 1.5 h and then cultured with or without PQ (750 μmol/L) for 24 h. Cell survival was determined using the MTT assay. Reactive oxygen species (ROS) production and Ca2+ levels were measured using flow cytometry. Glutathione reductase (GR) activity was determined using spectrophotometry. Expressions of the endoplasmic reticulum (ER) stress proteins, glucose regulatory protein 78 (Grp78) and C/EBP homologous protein (CHOP), were measured using Western blotting. Results Cell viability and GR activity were decreased, but ROS production, cytoplasmic Ca2+ levels, and expressions of Grp78 and CHOP were all increased in the PQ group compared to those in the control group. There were no statistically significant changes in the MnTMPyP group. Cell viability and GR activity were increased, while ROS production, cytoplasmic Ca2+ levels, and expressions of Grp78 and CHOP were all significantly reduced in the MnTMPyP group compared to those in the PQ group. Conclusion MnTMPyP effectively reduced PQ-induced lung epithelial-like cell injury, and the underlying mechanism is related to antagonism of PQ-induced ER stress and oxidative stress.关键词
MnTMPyP/百草枯/肺上皮细胞/氧化应激/内质网应激Key words
MnTMPyP/paraquat/lung epithelial-like cell/oxidative stress/endoplasmic reticulum stress分类
医药卫生引用本文复制引用
许勇民,孙大壮,宋春青,王蕊,董雪松..MnTMPyP通过抑制氧化应激和内质网应激减轻百草枯致肺上皮细胞损伤[J].中国医科大学学报,2019,48(1):1-6,6.基金项目
国家自然科学基金 (81471851) （81471851）
辽宁省博士启动基金 (20141033) （20141033）
