【摘要】 目的探讨大气细颗粒物PM2.5对肝细胞脂质代谢和氧化应激的影响。方法收集2014年广州城区大气中的PM2.5,以CCK-8法分析6.25~100μg/ml的PM2.5对肝L02细胞的毒性。根据PM2.5浓度分别设立6.25μg/ml组、12.50μg/ml组和25.00μg/ml组,同时设立阴性对照组,比较各组细胞内三酰甘油和胆固醇含量、肝X受体α(LXRα)和固醇调节元件结合蛋白-1c(SREBP-1c)的表达水平及氧自由基水平。结果 PM2.5浓度为50.00μg/ml时,对肝L02细胞有明显毒性。各剂量组肝细胞内的三酰甘油浓度显著高于阴性对照组,差异有统计学意义(P<0.05)。25.00μg/ml组的LXRα和SREBP-1c表达水平显著高于阴性对照组,差异有统计学意义(P<0.01)。各剂量组的氧自由基水平显著高于阴性对照组,差异有统计学意义(P<0.01)。结论 PM2.5可通过LXRα和SREBP-1c诱导肝细胞脂质堆积,并诱发肝细胞氧化应激,这可能是PM2.5引起非酒精性脂肪肝的重要机制。更多还原

【Abstract】 Objective To explore the influence of PM2.5 on lipid metabolism and oxidative stress of hepatocyte. Methods PM2.5 was collected from atmosphere in urban area of Guangzhou in 2014.Toxicity of liver L02 cell was analyzed by CCK-8 at PM2.5 levels of 6.25-100 μg/ml.The group of 6.25 μg/ml,12.5 μg/ml,25 μg/ml was set respectively,and the negative control group was set.The contents of intracellular triglyceride and cholesterol,the expression level of LXRα and SREBP-1c,the intracellular oxygen free radical level among four groups was compared. Results When the PM2.5 concentration was 50 g/ml,which had obvious toxicity to liver L02 cells.The concentration of triacylglycerol in the liver cells in each dose group was higher than that in the negative control group,with significant difference(P<0.05).The expression level of LXRα and SREBP-1c in the group of 25.00 g/ml was higher than that in the negative control group,with significant difference(P<0.01).The level of oxyradical in each dose group was higher than that in the negative control group,with significant difference(P<0.01). Conclusion PM2.5 can induce lipid accumulation in hepatocytes via LXRα and SREBP-1c,and induce oxidative stress in hepatocytes,which may be the important mechanism of PM2.5causing non-alcoholic fatty liver disease.更多还原