摘要
目的探讨交通相关的细颗粒物PM2.5对6T-CEM(人T淋巴细胞白血病细胞株)增殖抑制以及诱导凋亡的情况。方法采用四甲基偶氮唑兰(MTT)比色法测定不同浓度PM2.5对细胞24和48 h增殖功能的影响;FITC-AnnexinV/PI染色流式细胞仪测定交通相关细颗粒物染毒6T-CEM细胞的早期凋亡和坏死;罗丹明123法检测PM2.5对线粒体膜电位的影响。结果 160、320和800μg/ml PM2.5染毒细胞24 h与320和800μg/ml PM2.5染毒细胞48 h可抑制细胞增殖功能,与对照组比较有统计学意义(P<0.05);经FITC-Annexin V/PI染色流式细胞仪测定,320μg/mlPM2.5染毒细胞24 h后,细胞早期凋亡比生理盐水组升高,20、80和320μg/ml PM2.5染毒细胞48 h,细胞早期凋亡比生理盐水组升高,320μg/ml PM2.5染毒细胞24和48 h,细胞坏死比生理盐水组升高,差异有统计学意义(P<0.05);160和320μg/ml PM2.5染毒细胞24 h与80、160和320μg/ml PM2.5染毒细胞48 h线粒体膜电位与对照组比较有统计学差异(P<0.05)。结论交通相关的细颗粒物PM2.5对6T-CEM增殖功能有抑制作用,对细胞凋亡有一定的诱导作用,线粒体途径参与凋亡。
Objective To explore the proliferation function and apoptosis of 6T-CEM cells induced by traffic-related fine particles.Methods The effect of the proliferation function of 6T-CEM exposed to traffic-related PM2.5 for 24 or 48h was determined by MTT.Early apoptosis of and necrosis of 6T-CEM stained with FITC-Annexin-V/PI were detected by flow cytometry.The mitochondrial transmembrane potential of 6T-CEM was detected by flow Rh-123 single staining.Results The SI of 6T-CEM decreased markedly in both the 160,320,800 μg/ml PM2.5 groups after 24 h of PM2.5 exposure and 320,800 μg/ml groups after 48 h compared to control group,and the differences were statistically significant（P〈0.05）.After 24 h exposure,the early apoptosis rate of 6T-CEM in 320 μg/ml PM2.5 was higher than the control group and the difference of the late apoptosis and necrosis had no statistical significance.After 48 h exposure,the early apoptosis rates in 20,80,320 μg/ml PM2.5 were higher than the control group,and the late apoptosis and necrosis in 320 μg/ml PM2.5 were higher than the control group.There were significant differences bewteen above-mention＇d groups and control group（P〈0.05）.The mitochondrial transmembrane potential of 6T-CEM decreased in both the 160,320 μg/ml after 24h of PM2.5 exposure and 80,160,320 μg/ml groups after 48h exposure compared to control group（P〈0.05）.Conclusion The proliferation inhibition and induction of apoptosis of 6T-CEM could be caused by traffic-related fine particles,and the mitochondrial pathway might involve in the process of apoptosis.
出处
《毒理学杂志》
CAS
CSCD
北大核心
2011年第4期249-251,共3页
Journal of Toxicology
基金
国家自然科学基金(30700655)
山西省青年科技研究基金(2008021053)
山西高校科技研究开发项目(2007124)
2009年度山西省高等学校优秀青年学术带头人支持项目
关键词
PM2.5
早期凋亡
晚期凋亡
线粒体膜电位
PM2.5
early apoptosis
late apoptosis
mitochondrial transmembrane potential
