摘要
目的:观察太白楤木总皂苷对肝纤维化大鼠Smads4基因表达的影响。方法:CCl4诱导大鼠肝纤维化,以太白楤木总皂苷水溶液干预性治疗,Masson染色观察肝组织胶原沉积,ELISA法检测大鼠血清TGFβ1水平,原位杂交(in situ hybridization,ISH)和免疫组化(immunohistochemistry,IH)检测大鼠肝组织Smads4表达情况。结果:太白楤木总皂苷干预性治疗使肝纤维化大鼠血清TGFβ1水平明显下降[(51.2±18.6)vs(86.9±22.8)mg/L,P<0.05],肝脏胶原占肝组织面积比例减少;治疗组大鼠肝脏Smads4蛋白表达阳性率降低为(0.024±0.007)[模型组(0.135±0.086),P<0.01],Smads4 mRNA阳性率降低为(0.229±0.019)[模型组(0.723±0.090),P<0.01]。结论:太白楤木总皂苷可显著降低肝纤维化大鼠血清TGFβ1水平,减少肝胶原沉积,抑制肝脏Smads4表达,从而减弱了由TGFβ1介导的肝纤维化信号,可能是其发挥抗肝纤维化作用的分子机制之一。
Objective:To observe the effects of Aralia chinesis L Saponis on the expression of Smads4 gene in rats with CCl4-induced hepatic fihrosis and to investigate its probable molecular mechanisms in interfering liver fibrosis. Methods: Hepatil fihreosis in rats was induced by subcutaneous injection of CCl4. The expressions of Smads mRNA were detected with in situ hybridiza- tion (ISH) . The level of Smads4 protein in the liver tissue was detected with immunohistochemistry (IH) and the deposition of collagen in the liver was observed with HE and Masson staining. Results : The content of collagen obviously increased in the liver of model group and the expression of Smad4 mRNA in fibrotic liver was significantly enhanced. The positive ratio of Smad4 pro- tein significantly increased. All these increases were significantly decreased with Aralia chinesis L Saponis treatmcnt. Conclusion: Aralia chinesis L is effective in protecting rat liver against CCl4-induced hepatic fibrosis perhaps by inter fering the gene expression of Smads, which was essential in the fibrogenisis process of liver.
出处
《中西医结合肝病杂志》
CAS
2013年第2期93-94,共2页
Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases