薛彬,丁国斌,苏瑞军,晋小婷,李卓玉.大气细颗粒物暴露干扰心肌细胞存活和炎性反应的主要毒性组分研究[J].环境科学学报,2020,40(1):306-314
大气细颗粒物暴露干扰心肌细胞存活和炎性反应的主要毒性组分研究
- The main toxic components of fine particulate matters on cardiocytes: Focused on the cell viability and inflammatory response
- 基金项目：国家自然科学基金青年基金（No.21707085）；国家自然科学基金（No.31770382）；山西省青年科技基金（No.201701D221244）
- 丁国斌
- 山西大学生物技术研究所, 化学生物学与分子工程教育部重点实验室, 太原 030006
- 苏瑞军
- 山西大学生物技术研究所, 化学生物学与分子工程教育部重点实验室, 太原 030006
- 晋小婷
- 1. 山西大学生物医学研究院, 太原 030006;2. 中国科学院生态环境研究中心, 环境化学与生态毒理学国家重点实验室, 北京 100085
- 李卓玉
- 1. 山西大学生物技术研究所, 化学生物学与分子工程教育部重点实验室, 太原 030006;2. 山西大学生命科学院, 太原 030006
- 摘要：鉴于PM2.5组分呈现多样性和复杂性，其引起心力衰竭的主要毒性组分尚不清楚.由于采样地区、季节和污染源的不同，PM2.5不同组分的占比也会有巨大差异，但不同浓度无法比较其不同组分间的毒性差异.因此，为了揭示大气PM2.5引起心肌毒性作用的关键组分，分离复合型PM2.5的3种主要组分（有机组分、金属组分和水溶性组分），综合两种浓度暴露方式，即实际占比浓度和与复合型PM2.5相同的暴露浓度，染毒H9C2大鼠心肌细胞24 h和48 h，选择心肌细胞的细胞存活和炎症反应为主要评价指标，旨在揭示PM2.5对心肌造成毒性损伤的关键性成分.CCK-8法检测存活结果显示，不同组分在实际环境比重下，对心肌细胞存活率没有造成显著影响.相同浓度暴露下，高剂量组分（30 μg·cm-2）引起心肌细胞存活率显著降低，且有机组分毒性大于其他组分.根据细胞活力测定结果，选择低染毒浓度（10 μg·cm-2）暴露细胞，采用qRT-PCR和ELISA试剂盒检测炎症因子变化.与对照组相比，金属组暴露后，炎症因子TNF-α和IL-1β显著升高，而有机组则显著升高TNF-α的含量.结果表明，造成心肌细胞存活毒性和炎症损伤的主要PM2.5组分可能为有机组分和金属组分，而炎性反应对这两种组分的响应存在显著差异.
- Abstract：Considering the diversity and complexity of fine particulate matters (PM2.5), its key toxic components causing heart failure are still unclear. The differences of area, season and pollution source sampling PM2.5 lead to the huge discrepancies in the proportion of different components, which is the reason of why it is difficult to compare the myocardial toxicity among all kinds of components in a variety of concentrations. Hence, to investigate the key toxic components, the samples, including organic components of PM2.5(O-PM2.5), water-soluble components of PM2.5 (WS-PM2.5) and metal components of PM2.5 (M-PM2.5), were extracted from whole PM2.5 (W-PM2.5), and then exposed to H9C2 cells for 24 h and 48 h at two types of exposure concentrations (actual air proportion and the same concentrations of W-PM2.5). To identify the key toxic components of PM2.5, the effects of PM2.5 exposure on the cell viability and inflammatory were explored. The data from CCK-8 assay indicated that all components had no significant effect on the viability of myocardial cells in the actual air proportion. In the same concentrations, decreased viability was observed in the high dose (30 μg·cm-2) PM2.5-exposed H9C2 cells. Specially, the toxic of O-PM2.5 was higher than that of M-PM2.5. According to the above results, the expressions and activities of enzymes known to take part in heart failure were analyzed by qPCR and ELISA assay. The levels of TNF-α and IL-1β were conspicuously increased upon exposure to M-PM2.5 as compared with control group. Meanwhile, O-PM2.5 treatment remarkably caused the increase of TNF-α. These results demonstrated that O-PM2.5 and M-PM2.5 may be the key components to cause cardiotoxicity through the evaluation of viability and inflammation, and there is significant difference between O-PM2.5 and M-PM2.5 on inflammatory response.
