【摘要】 目的: 观察红景天甙对肝纤维化大鼠TGFβ- Smad通路的影响.方法: CCl4 诱导大鼠肝纤维化,以红景天甙水溶液干预性治疗,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(insituhybridization,ISH)和免疫组化(immunohistochemistry,IH)检测大鼠肝组织Smads表达情况.结果: 红景天甙干预性治疗使肝纤维化大鼠血清TGFβ1水平明显下降[ (53. 4±19 .5)vs(88. 7±22. 8)mg/L,P<0 .05 ],肝脏胶原占肝组织面积比例减少为( 0 .041±0 .011) [模型组(0 .167±0 .052),P<0 05];治疗组肝脏Smad4蛋白表达阳性率降低为(0. 023±0. 008) [模型组( 0 .137±0. 090),P< 0 .01 ],Smad4 mRNA阳性率降低为( 0 233±0 .018) [模型组( 0 .741±0. 091 ),P<0. 01 ];Smad7蛋白阳性率增加为( 0. 067±0 .010 ) [模型组( 0 .019±0. 002 ),P<0 .05 ],Smad7mRNA阳性率增加为( 0. 198±0. 011 )[模型组( 0 .074±0. 012 ),P<0 .01 ];肝组织Smads蛋白表达与SmadsmRNA水平变化一致.结论: 红景天甙防治可显著降低肝纤维化大鼠血清TGFβ1水平,减少肝脏胶原沉积,抑制肝脏Smad4表达及促进Smad7mRNA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.更多还原

【Abstract】 AIM: To observe the effects of salidroside on the expression of Smads gene in rats with CCl₄-induced hepatic fibrosis and to investigate its probable molecular mechanisms in interfering liver fibrosis.METHODS: Hepatic fibrosis in rats was induced by subcutaneous injection of CCl₄.The expressions of Smads mRNA were detected with in situ hybridization （ISH）.The level of Smads 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 Smad 4 mRNA in fibrotic liver was significantly enhanced.The positive ratio of Smad 4 protein significantly increased.All these increases were significantly decreased with salidroside treatment.However,the expression of Smad 7 in model group was very feeble but salidroside enhanced it obviously.CONCLUSION: Salidroside is effective in protecting rat liver against CCl₄-induced hepatic fibrosis perhaps by interfering the gene expression of Smads,which was essential in the fibrogenisis process of liver.更多还原