目的 研究三氯乙烯(TCE)致敏小鼠肝损伤过程中C3aR和C5aR蛋白及mRNA表达水平,探讨职业性三氯乙烯药疹样皮炎(DMLT)的发病机制.方法 将6-8周雌性BALB/c小鼠随机分成空白对照组(5只)、溶剂对照组(6只)和TCE处理组(65只),于第1、4、7、10天进行致敏,第17、19天进行激发,激发后24、48、72 h和7d处死动物,并记录体重和肝脏重量,无菌取出肝脏,用于病理观察组织结构,采用免疫荧光和实时荧光定量PCR检测C3aR和C5aR蛋白和mRNA表达水平.结果 未致敏组小鼠肝脏组织未见明显异常,TCE致敏组小鼠肝脏HE染色下观察可见明显的细胞排列疏松、细胞坏死和大量炎细胞浸润.24、48、72 h和7d致敏组中C3aR和C5aR蛋白和mRNA,表达水平明显高于空白对照组、溶剂对照组和相应时点的未致敏组,差异均有统计学意义(P<0.05).结论 TCE致敏小鼠肝损伤过程中有补体激活的参与,C3aR和C5aR可能发挥重要作用.
Objective To study the expression of C3aR and C5aR in trichloroethylene-sensitized mouse liver injury and discuss the pathogenesis of Dermatitis Medicamentosa-like of TCE (DMLT).Methods 6-8 w female BALB/c mouse were randomly divided into blank control group,solvent control group and TCE treatment group.TCE was given to the mouse for sensitization at 1th,4th,7th,10th day and challenge at 17th day and 19th day.Before killing mouse,liver weight and body weight were recorded.The livers were separated at 24 h,48 h,72 h and 7 d after challenge.And the liver sections were used for immunofluorescence stain and RT-PCR to detect the expression levels of C3aR and C5aR.Results Microscopic examination showed no significant change in liver structure or organization in TCE non-sensitized group,while liver cell oedema,cell necrosis and inflammatory cell infiltration were clearly observed in TCE-sensitized groups.The expression levels of C3aR and C5aR in 24 h,48 h,72 h and 7 d TCE-sensitized groups were significant higher than blank control group,solvent control group and related TCE non-sensitized groups (P〈0.05).Conclusion Complement activation was involved in TCE-induced liver injury and C3aR and C5aR might play essential role in the process.