论文部分内容阅读
目的观察自拟扶正消癌Ⅰ号方对大鼠肝纤维化实验模型转化生长因子β(TGF-β)和其下游Smad信号系统的作用,探讨该方对多种肿瘤的作用机制。方法采用SD大鼠,四氯化碳注射制作肝纤维化模型,采用扶正消癌Ⅰ号方灌胃,阳性对照药物为秋水仙碱,免疫组化法检测TGF-β,Western-blot方法检测Smad-3、Smad-7蛋白表达。结果与正常大鼠比较,模型组大鼠TGF-β表达显著升高(P<0.05),Smad-3呈高表达(P<0.05),Smad-7为低表达(P<0.05)。与模型组比较,扶正消癌Ⅰ号方组TGF-β和Smad-3的表达显著下降(P<0.05),Smad-7表达显著增强(P<0.05),显示该方对TGF-β、Smad-3、Smad-7表达较好的调节作用。结论扶正消癌Ⅰ号方对肝纤维化大鼠模型肝组织具有明显抑制TGF-β表达、下调Smad-3,上调Smad-7,对TGF-β-Smad系统具有较好的调节作用,可能是该方抗肝纤维化、抗肿瘤的机制之一。
Objective To observe the effect of Fuzheng Xiaohou Decoction Ⅰ on transforming growth factor-β (TGF-β) and its downstream Smad signaling system in rat model of hepatic fibrosis and to explore its mechanism of action on various tumors. Methods SD rats were injected with carbon tetrachloride to make hepatic fibrosis model. Fuzheng Xiaoyao Ⅰ was used for gavage. The positive control drug was colchicine, the expression of TGF-β was detected by immunohistochemistry and the expression of Smad -3, Smad-7 protein expression. Results Compared with normal rats, the expression of TGF-β in model group was significantly increased (P <0.05), Smad-3 was higher (P <0.05) and Smad-7 was lower (P <0.05). Compared with the model group, the expression of TGF-β and Smad-3 in Fuzheng Xiaohua Decoction Ⅰ group was significantly decreased (P <0.05) and the expression of Smad-7 was significantly increased (P <0.05) -3, Smad-7 expression better regulation. Conclusion Fuzheng Xiaohua Decoction Ⅰ can significantly inhibit the expression of TGF-β, down-regulate Smad-3 and up-regulate Smad-7 in hepatic tissue of liver fibrosis rats, which may be a good regulator of TGF-β-Smad system The party anti-liver fibrosis, one of the mechanisms of anti-tumor.