摘要
目的观察PM2.5暴露对非小细胞肺癌A549细胞的影响,进而了解其对细胞的毒性作用机制。方法利用细胞活力检测法确定PM2.5暴露的浓度;用透射电镜观察暴露后细胞的形态特征;通过转录组测序及实时定量RT-PCR,对损伤发生机制进行预测。结果通过细胞活力检测确定PM2.5暴露处理的终浓度为50μg/cm2。形态学检测表明,暴露处理后,细胞核内染色质凝聚,边集于核膜。凋亡相关基因IL1A、IL1B、CXCL3、CXCL2、PTGS2、IRAK2的表达上调,TP53和TNFRSF1A的表达下调。结论通过刺激细胞凋亡基因表达水平的变化,PM2.5暴露诱导了非小细胞肺癌A549细胞的凋亡。
Objective To observe the effects of PM2.5 exposure on A549 cells, and explore the mechanism of toxicity. Method The concentrations of PM2.5 exposure were determined utilizing cell viability assay. The morphological characteristics of exposed cell were observed with transmission electron microscope. Using big date from RNA-Seq and qRT-PCR, the mechanism was explored. Results The final concentration of PM2.5 exposure was 50 μg/cm2 ; morphological detection showed that chromatin condensation after exposure which was also found on the boundary of nuclear membrane. KEGG pathway analysis and interaction network were finished, and 8 kinds of apoptosis-related genes were found to be involved in the process of damage. Conclusion PM2.5 induces apoptosis in A549 cells by stimulating the changes of apoptosis-related genes expressions.
作者
杨彪
李新鸣
祁荣
陈冬梅
肖纯凌
YANG Biao LI Xinming QI Rong CHEN Dongmei XIAO Chunling(Basic Discipline of Chinese and Westem Integrative, Liaoning University of Traditional Chinese Medicine, Shenyang 110032, China Key Lab of Environmental Pollution and Mieroecology, Shenyang Medical College, Shenyang 110034, China Science Experiment Center, Shenyang Medical College, Shenyang 110032, China)
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2016年第12期1110-1114,共5页
Journal of China Medical University
基金
沈阳市重点实验室建设专项(No F14-181-1-00)
沈阳市科学技术计划(F13-221-9-36)
沈阳市公益类科技项目