三氯乙烯对小鼠肝脏PPARα和PPARγ表达的影响

Effects of trichloroethylene on the expression of liver PPARα and PPARγ in mice

目的探讨饮水摄入三氯乙烯(TCE)对小鼠肝脏过氧化物酶体增殖物活化受体(PPAR)α和PPARγ的影响。方法雌性BALB/c小鼠随机分为空白对照组、溶剂对照组、2.5 g/L TCE组和5.0 g/L TCE组,TCE经饮水暴露。分别在第2、4、8、12周时,取外周血检测肝功能;处死小鼠取肝脏组织,HE染色进行病理观察;分别采用实时荧光定量RT PCR法和免疫组化法检测PPARα和PPARγ的mRNA水平和蛋白表达。结果与空白对照组及溶剂对照组比较,2.5、5.0 g/L TCE组小鼠谷丙转氨酶(ALT)水平在第2、4周明显升高(P<0.05);HE染色显示2.5、5.0 g/L TCE组小鼠肝脏组织有明显炎细胞浸润及肝细胞变性,肝损伤在4周时最明显;与空白对照组及溶剂对照组比较,2.5、5.0 g/L TCE组小鼠肝脏中PPARα和PPARγmRNA表达量在4、8、12周时明显上升(P<0.05,P<0.01);2.5、5.0 g/L TCE组小鼠肝脏组织细胞核中均见PPARα和PPARγ的阳性表达,与空白对照组及溶剂对照组比较,各时期肝脏细胞核PPARα和PPARγ的阳性表达率显著上升(P<0.05)。结论饮水摄入TCE能上调小鼠肝脏PPARα和PPARγ表达。

Objective To investigate the effects of trichloroethylene（TCE） intake oxisome proliferator activated receptor （PPAR） α and PPARγ in mice. Methods via drinking water on liver per- The female BALB/c mice were randomly divided into blank control group, vehicle control group, 2.5 g/L TCE group and 5.0 g/L TCE group, and were exposed to TCE via drinking water. On the 2nd, 4th, 8th, 12th week, blood was collected for liver func- tion examination, liver tissues were taken for HE staining. The PPARα and PPARγ expression in liver were meas- ured by RT-PCR and immunohistochemical staining. Results The levels of ALT in 2.5, 5.0 g/L TCE treated groups increased significantly compared with control groups on the 2nd, 4th week （P 〈 0. 05 ） ; HE staining showed inflammatory cell infiltration and liver cell degeneration in 2. 5, 5.0 g/L TCE treated groups, the damage was most obvious on the 4th week; compared with control groups, PPARα and PPARγ mRNA expression in liver of TCE treated groups increased significantly on the 4th, 8th, 12th week （P 〈 0. 05, P 〈 0. 01 ） ; in the nuclei of liver cells, the expression of PPARα and PPARγ was positive in 2. 5, 5.0 g/L TCE treated groups, and the levels of PPARα and PPARγ expression in nuclei increased significantly compared with control groups on the 2nd, 4th, 8th, 12th week （P 〈0.05）. Conclusion The results suggest that TCE intake via drinking water can upregulate the ex- pression of liver PPARα and PPARγ in mice.