王吉耀 郭津生 刘淑玲 MarkA.Zern 200032，上海军医大学附属中山医院消化内科(王吉耀，郭津生，)

    Department of Midicine Pathologny，Jeffson Medicine Coloege，Philadelphia，Pennsylvania，USA(刘淑玲，Mark A.Zern) 中华肝脏病杂志 1999 0 7 1


    关键词：肝硬化 甘草甜素 核因子kB 期刊 zhgzbzz 0 基础研究 fur -->


    

摘要 目的 从分子水平探讨强力宁生物活性的发生机理。方法 大鼠随机分为正常对照组、模型对照组、强力宁组，后两组给予四氯化碳(CCl₄ )和乙醇造模处理以诱导慢性肝损伤，强力宁组在造模处理同时予强力宁治疗。各组大鼠在CCl₄ 等处理后第9周处死，收集血清和肝脏标本，测定血清ALT活性并进行组织学观察。部分肝组织提取细胞核蛋白进行凝胶迟滞实验以观察NF-kB活性。结果 CCl₄ 等处理后第9周模型对照组血清ALT水平显著高于强力宁组。模型大鼠肝脏脂肪变性和纤维化程度较强力宁治疗组更为严重。模型对照组肝脏内NF-kB活性较正常对照组显著增加，而强力宁组大鼠肝脏内NF-kB结合活性与正常组相接近。结论 强力宁能够抑制CCl₄ 联合乙醇诱导的慢性肝损伤大鼠肝脏内NF-kB的结合活性的增加，可能是强力宁具有保护肝毒素性肝损伤和纤维化作用的分子机制之一。

    

Inhibitory effect of glycyrrhizin on NF-kB binding activity in CCl4 plus ethanol induced liver cirrhosis in rats

WANG Jiyao,GUO Jinsheng,LIU Shuling,et al.

Department of Gastraenterology,ZhongShan Hospital,Shanghai Medical University,Shanghai 200032

Abstract Objective Toinvestigate the effects of Potenlini on nuclear factor-kB(NF-kB) binding activity in thelivers of animals models with liver cirrhosis,and to delineate the molecular mechanism ofthe bioactivities of Potenlini.Methods Male SD rats were randomlyallocated into a normal control group,a model control group,and a Potenlini group.Rats inthe latter two groups were treated with CCl₄ and Ethanol solution in order toinduce chronic liver injury.Rats in Potenlini group were given Potenlini treatment at thesame time.All rats were killed at thd 9th week after CCl₄ administration.Serumand liver specimens were collected,serum ALT activities and histological findings wereassessed.Nuclear extracts from liver tissues were prepared and gel retardation assays wereperformed for the evaluation of NF-kB activity.Results (1)Serum ALTlevels were significantly reduced in rats treated with Potenlini compared with those inrats of the model control group,which had dramatically increased ALTlevels.(2)Histologically,liver steatosis and fibrosis were severe in the rats of the modelgroup,but were significantly improved in rats of the Potenlini group.(3)NF-kB bindingactivity was markedly increased in the liver specimens taken from the rats of the modelcontrol group in comparison with the binding of normal livers,but the binding levels werenearly normal in the livers of the Potenlini group.Conclusion Potenlinican inhibit the NF-kB binding activity in CCl₄ and ethanol induced chronicliver injury,and that may partially be the mechanism by which Potenlini protects liverfrom hepatotoxin-induced liver injury and cirrhosis.

     ......