Combined exposure of fine particulate matter and high-fat diet aggravate the cardiac fibrosis in C57BL/6J mice

被引:41
作者
Jiang, Jinjin [1 ,2 ]
Li, Yang [1 ,2 ]
Liang, Shuang [1 ,2 ]
Sun, Baiyang [1 ,2 ]
Shi, Yanfeng [1 ,2 ]
Xu, Qing [3 ]
Zhang, Jie [4 ]
Shen, Heqing [4 ,5 ]
Duan, Junchao [1 ,2 ]
Sun, Zhiwei [1 ,2 ]
机构
[1] Capital Med Univ, Sch Publ Hlth, Dept Toxicol & Sanit Chem, Beijing 100069, Peoples R China
[2] Capital Med Univ, Beijing Key Lab Environm Toxicol, Beijing 100069, Peoples R China
[3] Capital Med Univ, Core Facil Ctr, Core Facil Electrophysiol, Beijing 100069, Peoples R China
[4] Xiamen Univ, Sch Publ Hlth, State Key Lab Mol Vaccinol & Mol Diagnost, Xiamen 361102, Peoples R China
[5] Chinese Acad Sci, Inst Urban Environm, Key Lab Urban Environm & Hlth, Xiamen 361021, Peoples R China
基金
中国国家自然科学基金;
关键词
Fine particulate matter; Combined exposure; Cardiac fibrosis; High-fat diet; ROS/TGF-beta; 1/Smad3; pathway; AIR-POLLUTION EXPOSURE; LONG-TERM EXPOSURE; OXIDATIVE STRESS; PM2.5; EXPOSURE; LUNG FIBROSIS; OBESITY; TOXICITY; INSIGHTS; ATHEROSCLEROSIS; ASSOCIATION;
D O I
10.1016/j.jhazmat.2020.122203
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Cardiac fibrosis is associated with fine particulate matter (PM2.5) exposure. In addition, whether high-fat diet (HFD) could exacerbate the PM2.5-induced cardiac injury was unevaluated. Thus, this study was aimed to investigate the combined effects of PM2.5 and HFD on cardiac fibrosis. The echocardiography and histopathological analysis showed that co-exposure of PM2.5 and HFD had a significant deleterious effect on both cardiac systolic and diastolic function accompanied the myofibril disorder and myocardial fibrosis in C57BL/6J mice than exposed to PM2.5 or HFD alone. The augmented oxidative damage and increased alpha-SMA area percentage were detected in heart tissue of mice exposed to PM2.5 and HFD together. PM2.5 upregulated the expressions of cardiac fibrosis-related special markers, including collagen-I, collagen-III, TGF-beta 1, p-Smad3 and total Smad3, which had more pronounced activations in co-exposure group. Meanwhile, the factorial analysis exhibited the synergistic interaction regarded to the combined exposure of PM2.5 and HFD. Simultaneously, PM2.5 and palmitic acid increased intracellular ROS generation and activated the TGF-beta 1/Smad3 signaling pathway in cardiomyocytes. While the ROS scavenger NAC had effectively attenuated the ROS level and suppressed the TGF-beta 1/Smad3 signaling pathway. Taken together, our results demonstrated combined exposure to PM2.5 and HFD could aggravate cardiac fibrosis via activating the ROS/TGF-beta 1/Smad3 signaling pathway.
引用
收藏
页数:15
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