摘要
目的:探讨角蛋白8在四氯化碳诱导的小鼠肝损伤中的表达和角蛋白8可能参与肝损伤过程的机制。方法:取ICR小鼠40只,分为4组,每组10只,雌雄各半。A组接受四氯化碳处理2周(6%的四氯化碳橄榄油溶液腹腔注射,300μl/kg体重,每周3次);B组接受四氯化碳处理4周;C组接受四氯化碳处理6周;D组为空白对照组。各组分别在最后一次注射四氯化碳的第3天,过量麻醉处死后取材。依次分离脾脏、双肾和心脏等重要脏器并称重。提取肝脏总RNA、RT-PCR和免疫组化方法检测角蛋白8的表达变化。结果:四氯化碳处理导致肝脏重量和体重的比值增高,第0、2、4和6周分别为5.60%、6.87%、7.83%和7.76%,差别具有统计学意义(P<0.01),脾脏重量和体重的比值也增高(P<0.05)。HE染色显示,肝损伤程度随四氯化碳处理时间延长而加重。RT-PCR和免疫组化检测发现,角蛋白8在肝脏的表达随四氯化碳处理时间延长而升高。结论:在四氯化碳诱导的小鼠肝损伤模型中,角蛋白8的表达水平和肝损伤程度在一定条件下呈正相关。角蛋白8的细胞内积累可能是肝损伤的分子机制之一。
Objective： To investigate the expression of keratin 8（K8） in carbon tetrachloride（CCl4）-induced liver injury of mice.Methods： Forty ICR mice were divided into four groups.CCl4 300 μl/kg body weight in olive oil was injected intraperitoneally for 0,2,4,6 weeks in group A,B,C and D,respectively.Mice were sacrificed 3 d after the last injection and then the vital organs were collected and weighed.RT-PCR and immunohistochemistry methods were used to analyze the expression of keratin 8 in the liver.Results： The ratios of liver and body weight were increased significantly after administration of CCl4,which were 5.60%,6.87%,7.83% and 7.76% at 0,2,4 and 6 weeks after injection,respectively.The expression of K8 was increased at the 2 w,4 w and 6 w after CL4 administration.Conclusions： The expression of K8 is positively correlated with the liver injury induced by CCl4.The accumulation of K8 may be involved in the mechanism of liver injury.
出处
《浙江大学学报（医学版）》
CAS
CSCD
北大核心
2010年第1期37-42,共6页
Journal of Zhejiang University(Medical Sciences)
基金
国家自然科学基金资助项目(30470089)
关键词
四氯化碳
角蛋白
免疫组织化学
疾病模型
动物
肝疾病
化学诱导
基因表达
Carbon tetrachloride
Keratin
Immunohistochemistry
Disease models
animal
Liver diseases/chem ind
Gene expression
