纤维连接蛋白对四氯化碳致小鼠急性肝损伤保护作用及其机制

Effect of fibronectin on carbon tetrachloride-induced acute hepatic damage in mice and its mechanism

目的探讨血浆纤维连接蛋白(fibronectin,FN)对急性肝损伤小鼠肝细胞的保护作用及其机制,为重型肝炎患者的治疗提供理论依据。方法昆明种小鼠20只随机分为对照组与肝损伤组,后者再分为治疗组与非治疗组。治疗组分别于注射CCl4前及注射后2,4,6 h尾静脉注射FN,非治疗组注射等量生理盐水,ELISA法检测肝组织TNF-α含量,免疫组化观察肝组织核转录因子κBp65表达情况,并进行比较。结果①非治疗组小鼠肝组织TNF-α含量显著高于治疗组(P<0.05);治疗组小鼠肝组织TNF-α含量与对照组比较无统计学意义(P>0.05)。②治疗组小鼠肝脏免疫组织化学核转录因子κBp65阳性率低于非治疗组。结论纤维连接蛋白可能通过降低四氯化碳致肝损伤小鼠肝脏TNF-α及核转录因子κBp65的过度表达而起保护作用。

Objective To investigate the effect of human plasma fibronectin（FN） on TNF-α content in liver tissues and expression of NFκBp65 in acute hepatic damage mice.Methods Twenty Kunming mice were randomized into 2 groups：control group and hepatic damage group.The mice were injected with CCl4 to induce the hepatic damage model in hepatic damage group,and the same volume of oil in control group.The model mice in hepatic damage group were subgrouped into treatment group and non-treatment group.The mice were given FN before and after the injection of CCl4 for 2,4,6 h in treatment group and the same volume of normal saline in non-treatment group.Enzyme-linked immunosorbent assay was used to detect the TNF-α content in liver tissues,and immunohistochemistry was applied to observe the expression of NFκBp65 in the liver of mice.Results ①The TNF-α content in liver tissues was significantly higher in non-treatment group than that in treatment group（P〈0.05）.The TNF-α content was not significantly different between control group and treatment group.②Immunohistochemical results showed that the positive rate of NFκBp65 in treatment group was significantly lower than in non-treatment group.Conclusion Fibronectin could prevent the liver failure by reducing the overexpression of TNF-α and NFκBp65 in carbon tetrachloride-induced liver necrosis.