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Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in human cardiomyocytes
Ecotoxicology and Environmental Safety ( IF 6.8 ) Pub Date : 2018-06-06 , DOI: 10.1016/j.ecoenv.2018.05.092
Xiaozhe Yang , Lin Feng , Yannan Zhang , Hejing Hu , Yanfeng Shi , Shuang Liang , Tong Zhao , Yang Fu , Junchao Duan , Zhiwei Sun

Although the strongly causal associations were between fine particulate matter (PM2.5) and cardiovascular disease, the toxic effect and potential mechanism of PM2.5 on heart was poorly understood. Thus, the aim of this study was to evaluate the cardiac toxicity of PM2.5 exposure on human cardiomyocytes (AC16). The cell viability was decreased while the LDH release was increased in a dose-dependent way after AC16 exposed to PM2.5. The reactive oxygen species (ROS) generation and production of malondialdehyde (MDA) were increased followed by the decreasing in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The damage of mitochondria was observed by ultra-structural analysis and MMP measurement. The apoptotic rate of AC16 were markedly elevated which was triggered by PM2.5. In addition, the proteins involved in mitochondria- mediated apoptosis pathway were measured. The protein levels of Caspase-3, Caspase-9 and Bax were up-regulated while the anti-apoptotic protein, Bcl-2 was down-regulated after AC16 exposed to PM2.5. In summary, our results demonstrated that mitochondria-mediated apoptosis pathway played a critical role in PM2.5-induced myocardial cytotoxicity in AC16, which suggested that PM2.5 may contribute to cardiac dysfunction.



中文翻译:

细粒物质(PM 2.5)通过线粒体介导的人心肌细胞凋亡途径诱导的细胞毒性

尽管细颗粒物(PM 2.5)与心血管疾病之间存在强烈的因果关系,但人们对PM 2.5对心脏的毒性作用和潜在机制的了解却很少。因此,本研究的目的是评估PM 2.5暴露对人心肌细胞(AC16)的心脏毒性。AC16暴露于PM 2.5后,细胞活力降低,而LDH释放以剂量依赖性方式增加。活性氧(ROS)的产生和丙二醛(MDA)的产生增加,其次是超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)减少。通过超结构分析和MMP测量观察线粒体的损​​伤。AC16的细胞凋亡率显着升高,其通过触发PM 2.5。另外,测量了在线粒体介导的细胞凋亡途径中涉及的蛋白质。AC16暴露于PM 2.5后,Caspase-3,Caspase-9和Bax的蛋白水平上调,而抗凋亡蛋白Bcl-2的水平下调。总之,我们的结果表明线粒体介导的凋亡途径在PM 2.5中起关键作用引起的AC16心肌细胞毒性,提示PM 2.5可能导致心脏功能障碍。

更新日期:2018-06-06
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