木疏胶囊抗大鼠肝纤维化机制研究

Antifibrotic effect of Mushu capsule in rats with hepatic fibrosis and its mechanism

目的通过观察木疏胶囊对肝纤维化大鼠纤维化相关基因表达的影响,探讨木疏胶囊抗肝纤维化分子水平的作用机制。方法 Wistar大鼠随机分为正常对照组,模型对照组,木疏胶囊预防组和治疗组,鳖甲软肝片预防组和治疗组。40%CCl4油溶液诱导大鼠肝纤维化模型。HE染色和Masson染色观察肝组织病理改变。RT-PCR法检测各组TGF-β1,α-SMA,col-Ⅰ,col-Ⅲ基因表达。结果 40%CCl4皮下注射诱导大鼠肝纤维化模型,病理观察证实造模成功。与模型对照组比较,各用药组各指标PCR产物均显著降低(P<0.01),木疏胶囊预防组分别与鳖甲软肝片预防组和治疗组比较显示TGF-β,α-SMA,col-Ⅰ,col-Ⅲ基因表达的降低均有统计学差异(P<0.01),木疏胶囊治疗组分别与鳖甲软肝片预防组和治疗组比较,TGF-β,α-SMA,col-Ⅰ,col-Ⅲ基因表达的降低均有统计学差异(P<0.05或P<0.01)。结论木疏胶囊预防和治疗用药均可使肝纤维化大鼠肝组织TGF-β1、α-SMA、Col-Ⅰ、Col-Ⅲ基因表达下降。

Objective To investigate the antifibrotic effect of Mushu capsule in rats with hepatic fibrosis and its molecular mechanism. Methods Wistar rats were randomly divided into 4 groups： normal control group,model group,Mushu capsule group（ MC） and Biejia Ruangan tablet group（ BRT） . MC group and BRT group were subdivided into prevention group and treatment group. A hepatic fibrosis model was induced by subcutaneous injection of 40% carbon tetrachloride（ CCl4） . Liver sections were stained with HE and Masson respectively for pathological observation. The gene expression of TGF-β1,α-SMA,col-Ⅰ,col-Ⅲ was detected by RT-PCR. Results The gene expression levels of TGF-β1,α-SMA,col-Ⅰand col-Ⅲ in model group were higher than that in normal control group（ P 0. 01） ,and all the expression levels in MC group and BRT group were significantly lower than that in model group（ P 0. 01） . Com- pared with BRT prevention group and treatment group,the gene expression of TGF-β1,α-SMA,col-Ⅰand col-Ⅲ in MC prevention group and treatment group decreased statistically（ P 0. 01 or P 0. 05） . Conclusion Mushu capsule has an antifibrotic effect in rats with liver fibrosis by decreasing the gene expression of TGF-β1,α-SMA,col-Ⅰ,col-Ⅲ.