TSP、PM_(2.5)致人脐静脉内皮细胞和人支气管上皮细胞氧化损伤及凋亡

Study on oxidative damage and apoptosis of human umbilical vein endothelial cells and human bronchial epithelial cells induced by particulatematters

研究环境空气与打印室内颗粒物(TSP、PM_(2.5))对人脐静脉内皮细胞(HUVEC)和人支气管上皮细胞(HBE)氧化损伤及凋亡的作用。将HUVEC和HBE分别暴露于100μg·mL^(-1)的环境空气TSP,打印室PM_(2.5)和环境空气PM_(2.5),采用CCK-8法检测细胞存活率,测定细胞中SOD活性和MDA含量,采用Western blot测定凋亡相关蛋白的表达。将HUVEC和HBE分别暴露于0,25,100,400μg·mL^(-1)的打印室PM_(2.5),采用CCK-8法检测细胞存活率,测定细胞中SOD活性和MDA含量,采用Western blot测定凋亡相关蛋白的表达。染毒7 h后,同一来源不同粒径的环境空气TSP和环境空气PM_(2.5)相比,环境空气PM_(2.5)能够显著降低HUVEC和HBE的细胞存活率和SOD活性,显著升高细胞中的MDA含量和凋亡通路中Bax/Bcl-2蛋白表达(P<0.05)。同一粒径不同来源的打印室PM_(2.5)和环境空气PM_(2.5)相比,环境空气PM_(2.5)显著降低HUVEC和HBE的细胞存活率和SOD活性,显著升高细胞中的MDA含量和凋亡通路中Bax/Bcl-2蛋白表达(P<0.05)。打印室PM_(2.5)亦显著降低HUVEC和HBE的细胞存活率和SOD活性,显著升高细胞中的MDA含量和凋亡通路中Bax/Bcl-2蛋白表达,并呈剂量-效应关系,浓度越高,作用效果越明显(P<0.05)。颗粒物粒径越小,诱导细胞氧化损伤和凋亡的能力越强;排放源是影响颗粒物毒性的重要因素之一;氧化损伤和线粒体凋亡途径是TSP、PM_(2.5)引起呼吸道疾病和心血管疾病的重要机制之一。

This paper studied the effects of ambient air and printing room particles on oxidative damage and apoptosis of human umbilical vein endothelial cells(HUVEC)and human bronchial epithelial cells(HBE).HUVEC and HBE were exposed to 100μg·mL^(-1) of ambient air TSP,printing room PM_(2.5) and ambient air PM_(2.5),respectively.Cell viability was measured by the cell counting kit-8(CCK-8)method,the superoxide dismutase(SOD)activity and the content of malondialdehyde(MDA)in the cells were determined,and the expression of apoptosis-related proteins were measured by western blot.HUVEC and HBE were exposed to PM_(2.5) at 0,25,100 and 400μg·mL^(-1),respectively.Cell viability was measured by the CCK-8 method,the SOD activity and MDA in the cells were measured,and the expression of apoptosis-related proteins were measured by western blot.After 7 hours of exposure,the ambient air TSP and ambient air PM_(2.5) from the same source can significantly reduce the cell viability and SOD activity of HUVEC and HBE,and can significantly increase the content of MDA and the expression of Bcl-2-associated X protein/B-cell lymphoma-2(Bax/Bcl-2)protein in the apoptosis pathway in cells.Printing room PM_(2.5) and ambient air PM_(2.5) from different sources of the same particle size,ambient air PM_(2.5) can significantly reduce the cell viability and SOD activity of HUVEC and HBE,and can significantly increase the content of MDA and the expression of Bax/Bcl-2 protein in the apoptosis pathway in cells.Printing room PM_(2.5) can significantly reduce the cell viability and SOD activity of HUVEC and HBE,and can significantly increase the content of MDA and the expression of Bax/Bcl-2 protein in the apoptosis pathway in cells,and it has a dose-response relationship.The smaller the particle size,the stronger the ability to induce cell oxidative damage and apoptosis.The emission source is one of the important factors affecting the toxicity of particulate matters.Oxidative damage and apoptosis are the important mechanisms that cause respiratory diseases and cardiovascular diseases caused by TSP and PM_(2.5).