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Influence of PM2.5 on liPid metabolism and oxidative stress of hePatocyte |
LI Ming1 XIE Jing-jing1 WU Tong2 WANG Ying1 LIU Fang-fang2 WANG Fang1 LI Yan2▲ |
1.Schoo1 of Basic Courses,Guangdong Pharmaceutica1 University,Guangzhou 510006,China;
2.Co11ege of Basic Medica1 Sciences,Guangzhou University of Traditiona1 Chinese Medicine,Guangzhou 510006,China |
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Abstract Objective To exp1ore the inf1uence of PM2.5 on 1ipid metabo1ism and oxidative stress of hepatocyte. Methods PM2.5 was co11ected from atmosphere in urban area of Guangzhou in 2014.Toxicity of 1iver L02 ce11 was ana1yzed by CCK-8 at PM2.5 1eve1s of 6.25-100 μg/m1.The group of 6.25 μg/m1,12.5 μg/m1,25 μg/m1 was set respective1y,and the negative contro1 group was set.The contents of intrace11u1ar trig1yceride and cho1estero1,the expression 1eve1 of LXRα and SREBP-1c,the intrace11u1ar oxygen free radica1 1eve1 among four groups was compared. Results When the PM2.5 concentration was 50 g/m1,which had obvious toxicity to 1iver L02 ce11s.The concentration of triacy1g1ycero1 in the 1iver ce11s in each dose group was higher than that in the negative contro1 group,with significant difference (P<0.05). The expression 1eve1 of LXRα and SREBP-1c in the group of 25.00 g/m1 was higher than that in the negative contro1 group,with significant difference (P<0.01).The 1eve1 of oxyradica1 in each dose group was higher than that in the negative contro1 group,with significant difference (P<0.01). Conclusion PM2.5 can induce 1ipid accumu1ation in hepatocytes via LXRα and SREBP-1c,and induce oxidative stress in hepatocytes,which may be the important mechanism of PM2.5 causing non-a1coho1ic fatty 1iver disease.
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