当前位置：
X-MOL 学术
›
Mutat. Res.
›
论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Ambient fine particulate matter (PM2.5) induces oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in human bronchial epithelial cells in vitro.
Mutation Research/Genetic Toxicology and Environmental Mutagenesis ( IF 1.9 ) Pub Date : 2019-02-13 , DOI: 10.1016/j.mrgentox.2018.12.005 Qi Yuan 1 , Yaoyao Chen 1 , Xiaobo Li 2 , Zhengdong Zhang 1 , Haiyan Chu 1
Mutation Research/Genetic Toxicology and Environmental Mutagenesis ( IF 1.9 ) Pub Date : 2019-02-13 , DOI: 10.1016/j.mrgentox.2018.12.005 Qi Yuan 1 , Yaoyao Chen 1 , Xiaobo Li 2 , Zhengdong Zhang 1 , Haiyan Chu 1
Affiliation
We investigated the mechanism responsible for the oxidative stress and pro-inflammatory response triggered by PM2.5 collected from Nanjing of China. Two human bronchial epithelia cell lines (HBE and BEAS-2B) were used. Human gene expression profile microarray was performed to investigate the alteration of gene expression in PM2.5-treated HBE cells. The results of ROS assay and ELISA indicated that PM2.5 (150 μg/ml) increased the level of cellular reactive oxygen species (ROS) and promoted the release of interleukin-6 (IL-6) in HBE cells. CYP1A1 and CYP1B1 were the top two up-regulated genes by PM2.5 (150 μg/ml, 48 h of exposure) in HBE cells. Co-knockdown of CYP1A1/1B1 by siRNA substantially inhibited PM2.5-induced ROS generation, IL-6/IL-8 secretion and STAT3/P-STAT3 expression. Similarly, the knockdown of STAT3 also effectively inhibited PM2.5-induced rise in ROS level and IL-6/IL-8 secretion. In summary, PM2.5 mediated oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in two human bronchial epithelial cell lines.
更新日期：2019-11-01
京公网安备 11010802027423号