• 关键词：PM_2.5  肺上皮细胞  氧化应激  COPD

• 基金项目：苏州市科技支撑计划项目（No.SS201445）

• 孙哲琳
• 1. 上海大学生命科学学院, 上海 200444;2. 中国科学院苏州纳米技术与纳米仿生研究所, 苏州 215123

• 陈重军
• 苏州科技学院, 苏州 215009

• 杨令延
• 中国科学院苏州纳米技术与纳米仿生研究所, 苏州 215123

• 邹强
• 苏州环境监测中心, 苏州 215004

• 索广力
• 中国科学院苏州纳米技术与纳米仿生研究所, 苏州 215123

• 黄俊逸
• 上海大学生命科学学院, 上海 200444

• 林家骅
• 中国科学院苏州纳米技术与纳米仿生研究所, 苏州 215123

• 摘要：为了检测大气PM_2.5对正常肺上皮细胞（BEAS-2B）的损伤作用和慢性阻塞性肺病（COPD）相关基因及蛋白的表达变化，将PM_2.5的不同组分对肺上皮细胞进行染毒24 h后，通过MTT、荧光探针、Western Blot、单细胞凝胶电泳、实时荧光定量PCR、ELISA等方法检测细胞损伤、COPD相关基因和蛋白表达的变化情况.结果发现，PM_2.5可造成肺上皮细胞活性降低，且呈剂量依赖性，PM_2.5的不同组分对细胞造成的损伤也不同，有机相组分在细胞凋亡、紧密连接蛋白表达量、DNA损伤和炎症反应等方面造成的影响都比水相组分严重，而水相组分在氧化应激反应和COPD相关蛋白变化程度方面的作用都高于有机相组分.由此可见，PM_2.5可对肺上皮细胞造成多种不同程度、不同水平的损伤作用，其中，氧化应激可能是影响COPD相关基因和蛋白表达的重要因素.

• Abstract：To estimate the damage level of human lung epithelial cell and the attack rate of chronic obstructive pulmonary disease(COPD) caused by different extracts from ambient particulate matter 2.5(PM_2.5), we used the human lung epithelial cell line BEAS-2B to define the association between COPD biomarkers and PM_2.5. After 24 h exposure of PM_2.5 to the epithelial cell line, the experiments of MTT, fluorescent probe technique, single cell gel electrophoresis, qPCR, and ELISA were performed to estimate the cell damages. We found that PM_2.5 caused the decrease in cell viability in a dose-dependent manner. The damage level caused by PM_2.5 extracts was different between organic and water-soluble extract. These results suggested that PM_2.5 can damage cell in several different ways. PM_2.5 may cause cell death, DNA damage and inflammation, induce oxidative stress response, and change the expression of tight junction proteins and COPD biomarkers. The damage caused by organic and water-soluble parts of PM_2.5 was substantial and diverse. Oxidative stress may be the primary mechanism of COPD biomarkers caused by PM_2.5.

• Key words：PM_2.5  lung epithelial cell  oxidative stress  COPD

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