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Selenomethionine mitigate PM2.5-induced cellular senescence in the lung via attenuating inflammatory response mediated by cGAS/STING/ NF-?B pathway

文献类型： 外文期刊

作者： Wang, Xiaofei 1 ; Lu, Wenzun 1 ; Xia, Xuanyi 1 ; Zhu, Yuchen 1 ; Ge, Chunmei 1 ; Guo, Xiaoying 3 ; Zhang, Ning 1 ; Chen, Hua 1 ; Xu, Shengmin 2 ;

作者机构： 1.Hefei Univ, Sch Biol Food & Environm, Hefei 230601, Peoples R China

2.Anhui Univ, Informat Mat & Intelligent Sensing Lab Anhui Prov, Hefei 230601, Peoples R China

3.Anhui Acad Agr Sci, Inst Agr Engn, Hefei 230031, Peoples R China

4.Jinxiu Ave 99, Hefei 230601, Anhui, Peoples R China

5.Jiulong Rd 111, Hefei 230601, Anhui, Peoples R China

关键词： Particulate matter 2; 5 (PM2; 5); Inflammation; Senescence; Selenomethionine; Cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase  (cGAS)

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：7.129； 五年影响因子：7.284 ）

ISSN： 0147-6513

年卷期： 2022 年 247 卷

页码：

收录情况： SCI

摘要： Particulate matter 2.5 (PM2.5) is a widely known atmospheric pollutant which can induce the aging-related pulmonary diseases such as acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary dis-ease (COPD) and interstitial pulmonary fibrosis (IPF). In recent years, with the increasing atmospheric pollution, airborne fine PM2.5, which is an integral part of air pollutants, has become a thorny problem. Hence, this study focused on the effect of PM2.5 on cellular senescence in the lung, identifying which inflammatory pathway mediated PM2.5-induced cellular senescence and how to play a protective role against this issue. Our data suggested that PM2.5 induced time-and concentration-dependent increasement in the senescence of A549 cells. Using an inhibitor of cGAS (PF-06928215) and an inhibitor of NF-kappa B (BAY 11-7082), it was revealed that PM2.5-induced senescence was regulated by inflammatory response, which was closely related to the cGAS/STING/NF-kappa B pathway activated by DNA damage. Moreover, our study also showed that the pretreatment with seleno-methionine (Se-Met) could inhibit inflammatory response and prevent cellular senescence by hindering cGAS/ STING/NF-kappa B pathway in A549 cells exposed to PM2.5. Furthermore, in vivo C57BL/6J mice model demonstrated that aging of mouse lung tissue caused by PM2.5 was attenuated by decreasing cGAS expression after Se-Met treatment. Our findings indicated that selenium made a defense capability for PM2.5-induced cellular senes-cence in the lung, which provided a novel insight for resisting the harm of PM2.5 to human health.

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