愈肝颗粒抗肝纤维化及其对Smad4、Smad7影响的实验研究

目的观察愈肝颗粒抗实验性大鼠肝纤维化的疗效及作用机制。方法二甲基亚硝胺诱导大鼠肝纤维化模型,以愈肝颗粒浸膏灌胃进行治疗。HE染色观测肝组织病理学变化并进行肝脏炎症活动度和纤维化程度计分,免疫组化检测Smad4和Smad7在肝内的表达及分布的变化,并用图像分析软件对它们表达的阳性区域面积及光密度进行半定量分析。结果愈肝颗粒组与模型对照组比较：组织病理学显示肝脏炎症及纤维化减轻。炎症活动度和纤维化程度计分明显降低。免疫组化中Smad4表达减少,阳性染色面积（PA）及光密度值（OD）降低,Smad7表达明显增多,PA及OD值增加,P值均〈0.01。结论愈肝颗粒能明显减轻肝脏炎症、坏死及肝纤维化,其作用机制与其下调Smad4,上调Smad7,重建R-Smad/I-Smad平衡有关。

EXPERIMENTAL STUDY OF YUGANKELI ON LIVER FIBROSIS ANIAGONIZING AND SMAD4,SMAD7 EXPRESSION

Objective To explore the efficacy and possible mechanism of YuGanKeLi （YGKL） antagonizing experimental hepatic fibrosis model in rats. Methods The hepatic fibrosis model in rats was induced by dimethylnitrosamine （DMN）, which was treated with YuGanKeLi （YGKL） extractum by gavage. The pathological changes of liver was observed with HE staining and the scores of liver inflammation activity and fibrosis degree were evaluated. In addition, the expression of Smad4 and Smad7 in liver was detected by immunohistochemistry, and an image semiquantitative analysis system was used to analyze the positive area （PA） and optical density （OD）. Results Compared YGKL groups with control groups, it showed that .. the inflammation and fibrosis were lessened in pathological sections; the scores of liver inflammation activity and fibrosis degree lowered significantly; the expression of Smad4 decreased significantly in immunohistochemistry, while the Smad7 expressed increased significantly （ P%0.01 ）. Conclusion YGKL has a better curative efficacy in reducing the inflammation, necrosis and collagen fibers proliferation in rats probably because it can increase the expression of Smad7 while decrease that of Smad4 and finally rebuilt the balance between Smad4 and Smad7.