环境细颗粒物（PM）在体外通过上调人支气管上皮细胞中CYP1A1/1B1的表达诱导氧化应激和促炎反应。
Ambient fine particulate matter (PM) induces oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in human bronchial epithelial cells in vitro.
作者信息
Yuan Qi, Chen Yaoyao, Li Xiaobo, Zhang Zhengdong, Chu Haiyan
机构信息
Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China; Department of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, China.
出版信息
Mutat Res Genet Toxicol Environ Mutagen. 2019 Mar;839:40-48. doi: 10.1016/j.mrgentox.2018.12.005. Epub 2018 Dec 12.
We investigated the mechanism responsible for the oxidative stress and pro-inflammatory response triggered by PM 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 PM-treated HBE cells. The results of ROS assay and ELISA indicated that PM (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 PM (150 μg/ml, 48 h of exposure) in HBE cells. Co-knockdown of CYP1A1/1B1 by siRNA substantially inhibited PM-induced ROS generation, IL-6/IL-8 secretion and STAT3/P-STAT3 expression. Similarly, the knockdown of STAT3 also effectively inhibited PM-induced rise in ROS level and IL-6/IL-8 secretion. In summary, PM mediated oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in two human bronchial epithelial cell lines.
我们研究了从中国南京采集的颗粒物（PM）引发氧化应激和促炎反应的机制。使用了两个人类支气管上皮细胞系（HBE和BEAS-2B）。进行人类基因表达谱微阵列分析以研究经PM处理的HBE细胞中的基因表达变化。活性氧（ROS）检测和酶联免疫吸附测定（ELISA）结果表明，PM（150μg/ml）可增加HBE细胞中的细胞活性氧水平，并促进白细胞介素-6（IL-6）的释放。CYP1A1和CYP1B1是HBE细胞中经PM（150μg/ml，暴露48小时）上调最显著的两个基因。通过小干扰RNA（siRNA）共敲低CYP1A1/1B1可显著抑制PM诱导的ROS生成、IL-6/IL-8分泌以及信号转导和转录激活因子3（STAT3）/磷酸化STAT3（P-STAT3）的表达。同样，敲低STAT3也有效抑制了PM诱导的ROS水平升高和IL-6/IL-8分泌。总之，在两个人类支气管上皮细胞系中，PM通过上调CYP1A1/1B1的表达介导氧化应激和促炎反应。
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