摘 要目的:通过观察肝组织IkB表达情况，探讨黄芪抗肝纤维化机制。方法:SD大鼠随机分为正常对照组、CCl4诱导肝纤维化组和黄芪干预组。采用HE染色以及Ⅰ型胶原染色评价各组肝纤维化程度，免疫组化方法检测NF-kB和IkBa在肝组织中表达。结果:肝纤维化组的肝纤维化分级明显高于正常对照组(P<0.01)，黄芪干预组肝纤维化分级与肝纤维化组比较明显降低(P<0.01)。肝纤维化组大鼠肝组织NF-kB、IkBa表达均显著高于正常对照组(P<0.01)，黄芪组NF-kB表达较肝纤维化组显著降低(P<0.01)，IkB表达较肝纤维化组明显升高(P<0.05)。结论:黄芪可以显著抑制CCl4诱导的肝纤维化，对IkBa表达的调控可能是其机制之一。

    关键词黄芪；肝纤维化；IkBa； 核因子-kB

    中图分类号:R573.3+2 文献标识码: A

    AbstractObjective：To explore the effect of astragalus on rat model of liver fribrosis by detecting the expression of IkB in liver tissue. Methods：SD rats were randomly divided into normal control group, carbon tetrachloride (CCl4)-induced liver fibrosis group and Astragalus group. Type Ⅰ collagen and HE staining were used to evaluate the grade of liver fibrosis. Immunohistochemistry was used to detect the expression of IkBa and NF-kB in liver tissue. Results：The degree of liver fibrosis in fibrosis group was significantly higher than that in the normal control group (P<0.01), which was decreased remarkably by Astragalus treatment (P<0.01). The expression of IkBa and NF-kB in fibrosis group was significantly higher than that in the normal control group (P<0.01). Compared to liver fibrosis group, the expression of NF-kB was significantly reduced (P<0.01), while the expression of IkB was upregulated remarkably (P<0.05) in Astragalus group. Conclusion：In this CCl4-induced rat model, liver fibrosis was inhibited by Astragalus. The inhibitory effect of Astragalus on liver fibrosis might be related to the upregulation of IkBa. ......