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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，后两组给子四氯化碳（ＣＣ１４）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ＣＣ１４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ＣＣ１４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－ＸＢ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ＣＣ１４联会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。
From the molecular level to explore the mechanism of strong biological activity rather than. Methods The rats were randomly divided into normal control group, model control group, Qiangli Ning group, and the latter two groups were given CCl4 and ethanol to induce chronic liver injury. Strong rather treatment. Rats in each group were sacrificed at 9 weeks after CC14 treatment. Serum and liver samples were collected, serum ALT activity was measured and histological observation was performed. Part of the liver tissue extracted nuclear protein gel retardation experiment to observe NF-KB activity. Results The level of serum ALT in model control group after 9 weeks of CC14 treatment was significantly higher than that of Qiangli Ning group. Model rats liver steatosis and fibrosis more powerful Ning treatment group more serious. The activity of NF-XB in the liver of the model control group was significantly increased compared with the normal control group, while the NF-κB binding activity in the liver of the Qianglinning group was similar to that of the normal group. CONCLUSION: Qiangningning can inhibit the increase of NF-kB binding activity in the liver of rats with CCI-induced chronic liver injury induced by CC14, which may be one of the molecular mechanisms of its protective effect on hepatic hepatotoxicity and fibrosis.