夏季和冬季大气PM_(2.5)水溶性颗粒物与总颗粒物对BEAS-2B细胞活性与炎症的影响
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摘要
目的探讨夏季与冬季的大气颗粒物PM_(2.5)水溶性成分与总颗粒物对BEAS-2B细胞的细胞活性与炎症的影响。方法将夏季和冬季采集的PM_(2.5)分别提取水溶性成分与总颗粒物,得到4种PM_(2.5)组分,使用CCK-8法检测25、50、100、200、400μg/ml PM_(2.5)暴露细胞后的细胞活性;以100μg/ml PM_(2.5)处理细胞12、24、48 h后提取RNA,用qRT-PCR技术检测IL-1α、IL-1β、IL-6、IL-8炎症因子与炎症小体NLRP3及caspase-1、IL-18的水平。结果夏季和冬季PM_(2.5)的水溶性成分与总颗粒物分别处理细胞12 h后,部分剂量组细胞活性升高,随着PM_(2.5)暴露时间的增加,细胞活性逐渐得到抑制,差异具有统计学意义(P<0.05)。100μg/ml的PM_(2.5)处理细胞后,IL-1α和IL-1β表达水平高于IL-6和IL-8;炎症小体NLRP3、caspase-1和IL-18在100μg/ml的PM_(2.5)处理24、48 h后也呈现升高趋势,差异具有统计学意义(P<0.05)。结论夏季和冬季PM_(2.5)水溶性成分与总颗粒物可以抑制细胞活性,并且促使细胞炎症发生,冬季总颗粒物对细胞活性与炎症的影响更明显。
Objective To understand the effects of water-soluble components and total particulate matter of PM_(2.5) collected in summer and winter on cell viability and inflammation of BEAS-2B cells. Methods Four kinds of PM_(2.5) components were obtained by extracting water-soluble components and total particulate matter from PM_(2.5) collected in summer and winter respectively. The cell viability was determined by using CCK-8 kit after treated with PM_(2.5) at the doses of 25,50,100,200 and400 μg/ml respectively. RNA was extracted and the levels of inflammatory cytokines IL-1α,IL-1β,IL-6,IL-8,and NLRP3 inflammatory body,caspase-1 and IL-18 were detected by q RT-PCR after 12 h-,24 h-and 48 h-treatment with 100 μg/ml PM_(2.5),respectively. Results The cell viabilities increased after 12 h-treatment with water-soluble components and total particulate matter of PM_(2.5) at some exposure doses,and as the exposure time increased,the cell viability was gradually inhibited,the difference was statistically significant(P<0.05). The expression levels of IL-1α and IL-1β were higher than IL-6 and IL-8 in BEAS-2 B cells exposed to 100 μg/ml PM_(2.5). Inflammatory body NLRP3 and its related molecules(caspase-1 and IL-18) also showed an increasing trend after PM_(2.5) treatment at 100 μg/ml for 24 h and 48 h respectively,the difference was statistically significant(P<0.05). Conclusion The water-soluble components and total particulate matter of PM_(2.5) in summer and winter can inhibit cell viability and promote cell inflammation,and total particulate matter of PM_(2.5) in winter has a greater adverse effects.
Objective To understand the effects of water-soluble components and total particulate matter of PM_(2.5) collected in summer and winter on cell viability and inflammation of BEAS-2B cells. Methods Four kinds of PM_(2.5) components were obtained by extracting water-soluble components and total particulate matter from PM_(2.5) collected in summer and winter respectively. The cell viability was determined by using CCK-8 kit after treated with PM_(2.5) at the doses of 25,50,100,200 and400 μg/ml respectively. RNA was extracted and the levels of inflammatory cytokines IL-1α,IL-1β,IL-6,IL-8,and NLRP3 inflammatory body,caspase-1 and IL-18 were detected by q RT-PCR after 12 h-,24 h-and 48 h-treatment with 100 μg/ml PM_(2.5),respectively. Results The cell viabilities increased after 12 h-treatment with water-soluble components and total particulate matter of PM_(2.5) at some exposure doses,and as the exposure time increased,the cell viability was gradually inhibited,the difference was statistically significant(P<0.05). The expression levels of IL-1α and IL-1β were higher than IL-6 and IL-8 in BEAS-2 B cells exposed to 100 μg/ml PM_(2.5). Inflammatory body NLRP3 and its related molecules(caspase-1 and IL-18) also showed an increasing trend after PM_(2.5) treatment at 100 μg/ml for 24 h and 48 h respectively,the difference was statistically significant(P<0.05). Conclusion The water-soluble components and total particulate matter of PM_(2.5) in summer and winter can inhibit cell viability and promote cell inflammation,and total particulate matter of PM_(2.5) in winter has a greater adverse effects.
引文
[1]Yang Q,Yuan Q,Li T,et al.The relationships between PM2.5and meteorological factors in China:seasonal and regional variations[J].Int J Environ Res Public Health.2017,14:1510.
[2]Chen Y,Luo XS,Zhao Z,et al.Summer-winter differences of PM2.5toxicity to human alveolar epithelial cells(A549)and the roles of transition metals[J].Ecotoxicol Environ Saf,2018,165:505-509.
[3]Chen M,Li B,Sang N.Particulate matter(PM2.5)exposure seasondependently induces neuronal apoptosis and synaptic injuries[J].JEnviron Sci(China),2017,54:336-345.
[4]李丽平.青岛大气PM2.5中水溶性无机离子及其前体气体的浓度特征和气-粒平衡关系[D].青岛：中国海洋大学，2014.
[5]Mirabelli MC,Vaidyanathan A,Flanders WD,et al.Outdoor PM2.5,ambient air temperature,and asthma symptoms in the past 14 days among adults with active asthma[J].Environ Health Perspect.2016,124:1882-1890.
[6]Sunyer J,Jarvis D,Gotschi T,et al.Chronic bronchitis and urban air pollution in an international study[J].Occup Environ Med.2006,63:836-843.
[7]Zheng Z,Zhang X,Wang J,et al.Exposure to fine airborne particulate matters induces hepatic fibrosis in murine models[J].JHepatol.2015,63:1397-1404.
[8]Sun XW,Chen PL,Ren L,et al.The cumulative effect of air pollutants on the acute exacerbation of COPD in Shanghai,China[J].Sci Total Environ,2018,622-623:875-881.
[9]Zou Y,Jin C,Su Y,et al.Water soluble and insoluble components of urban PM2.5and their cytotoxic effects on epithelial cells(A549)in vitro[J].Environ Pollut,2016,212:627-635.
[10]Zhao C,Niu M,Song S,et al.Serum metabolomics analysis of mice that received repeated airway exposure to a water-soluble PM2.5extract[J].Ecotoxicol Environ Saf,2019,168:102-109.
[11]Long F,Jiang H,Yi H,et al.Particulate matter 2.5 induced bronchial epithelial cell injury via activation of 5’-adenosine monophosphateactivated protein kinase-mediated autophagy[J].J Cell Biochem.2018.doi.org/10.1002/jcb.27597.
[12]Ma QY,Huang DY,Zhang HJ,et al.Exposure to particulate matter2.5(PM2.5)induced macrophage-dependent inflammation,characterized by increased Th1/Th17 cytokine secretion and cytotoxicity[J].Int Immunopharmacol,2017,50:139-145.
[13]Wang H,Song L,Ju W,et al.The acute airway inflammation induced by PM2.5exposure and the treatment of essential oils in BALB/c mice[J].Sci Rep,2017,7:44256.
[14]Wang B R,Shi J Q,Ge N N,et al.PM2.5exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer’s disease[J].J Neuroinflammation,2018,15:132.
[15]Zheng R,Tao L,Jian H,et al.NLRP3 inflammasome activation and lung fibrosis caused by airborne fine particulate matter[J].Ecotoxicol Environ Saf,2018,163:612-619.
[2]Chen Y,Luo XS,Zhao Z,et al.Summer-winter differences of PM2.5toxicity to human alveolar epithelial cells(A549)and the roles of transition metals[J].Ecotoxicol Environ Saf,2018,165:505-509.
[3]Chen M,Li B,Sang N.Particulate matter(PM2.5)exposure seasondependently induces neuronal apoptosis and synaptic injuries[J].JEnviron Sci(China),2017,54:336-345.
[4]李丽平.青岛大气PM2.5中水溶性无机离子及其前体气体的浓度特征和气-粒平衡关系[D].青岛：中国海洋大学，2014.
[5]Mirabelli MC,Vaidyanathan A,Flanders WD,et al.Outdoor PM2.5,ambient air temperature,and asthma symptoms in the past 14 days among adults with active asthma[J].Environ Health Perspect.2016,124:1882-1890.
[6]Sunyer J,Jarvis D,Gotschi T,et al.Chronic bronchitis and urban air pollution in an international study[J].Occup Environ Med.2006,63:836-843.
[7]Zheng Z,Zhang X,Wang J,et al.Exposure to fine airborne particulate matters induces hepatic fibrosis in murine models[J].JHepatol.2015,63:1397-1404.
[8]Sun XW,Chen PL,Ren L,et al.The cumulative effect of air pollutants on the acute exacerbation of COPD in Shanghai,China[J].Sci Total Environ,2018,622-623:875-881.
[9]Zou Y,Jin C,Su Y,et al.Water soluble and insoluble components of urban PM2.5and their cytotoxic effects on epithelial cells(A549)in vitro[J].Environ Pollut,2016,212:627-635.
[10]Zhao C,Niu M,Song S,et al.Serum metabolomics analysis of mice that received repeated airway exposure to a water-soluble PM2.5extract[J].Ecotoxicol Environ Saf,2019,168:102-109.
[11]Long F,Jiang H,Yi H,et al.Particulate matter 2.5 induced bronchial epithelial cell injury via activation of 5’-adenosine monophosphateactivated protein kinase-mediated autophagy[J].J Cell Biochem.2018.doi.org/10.1002/jcb.27597.
[12]Ma QY,Huang DY,Zhang HJ,et al.Exposure to particulate matter2.5(PM2.5)induced macrophage-dependent inflammation,characterized by increased Th1/Th17 cytokine secretion and cytotoxicity[J].Int Immunopharmacol,2017,50:139-145.
[13]Wang H,Song L,Ju W,et al.The acute airway inflammation induced by PM2.5exposure and the treatment of essential oils in BALB/c mice[J].Sci Rep,2017,7:44256.
[14]Wang B R,Shi J Q,Ge N N,et al.PM2.5exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer’s disease[J].J Neuroinflammation,2018,15:132.
[15]Zheng R,Tao L,Jian H,et al.NLRP3 inflammasome activation and lung fibrosis caused by airborne fine particulate matter[J].Ecotoxicol Environ Saf,2018,163:612-619.
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