【摘要】 目的探讨水飞蓟素抗CCl4和酒精所致肝纤维化的作用和机制。方法50只♂昆明小鼠随机分为5组,模型组小鼠皮下注射CCl4并饮用酒精制造肝纤维化模型,治疗组以低、中、高3种不同浓度(50、100、200mg.kg-1)的水飞蓟素灌胃进行干预,正常组小鼠皮下注射等量植物油并用生理盐水灌胃。通过检测血清AST、ALT水平、肝脏病理组织学变化、肝脏组织转化生长因子-β1(TGF-β1)、α-肌动蛋白(α-SMA)及Ⅰ型胶原(collagen-Ⅰ)mRNA表达水平观察水飞蓟素的疗效。结果成功建立肝纤维化模型,模型组小鼠血清AST、ALT,肝脏组织TGF-β1、α-SMA及collagen-ⅠmR-NA表达水平增高,水飞蓟素可降低血清AST、ALT水平,降低肝组织TGF-β1、α-SMA及collagen-ⅠmRNA的表达,减轻肝纤维化程度,中剂量(100mg.kg-1)疗效最好。结论水飞蓟素对酒精和CCl4所致的肝脏损伤有明显保护作用,其机制可能与降低TGF-β1mRNA的表达、抑制肝星状细胞(hepatic stellate cells,HSC)活化有关。更多还原

【Abstract】 Aim To observe the anti-fibrosis effect and mechanism of Silymarin(SIL) on mice hepatic fibrosis caused by alcohol and CCl4.Methods 50 Kunming mice were randomly divided into 5 groups.Fibrosis model group was given CCl4 through subcutaneous injections plus alcohol oral administration.The treated groups were divided into low dose(50 mg·kg-1 body weight),medium dose(100 mg·kg-1 body weight),high dose(200 mg·kg-1 body weight) of SIL and normal group was given plant oil through subcutaneous injections and physiological saline oral administration.All groups were raised for 8 weeks.ALT and AST of serum,the histopathology of the mice liver and the mRNA expression of TGF-β1,α-SMA and collagen-Ⅰwere detected.Results The hepatic fibrosis mice models were successfully made,the level of serum AST,ALT and TGF-β1,α-SMA and collagen-Ⅰ mRNA of liver were increased in model groups,SIL decreased the level of serum ALT,AST and the expression of TGF-β1,α-SMA and collagen-Ⅰ mRNA,the medium dose of SIL had the most significant effect.Conclusion SIL significantly reduces alcohol and CCl4-induced mice hepatic fibrosis,probably by reducing the expression of TGF-β1 mRNA and then inhibiting the proliferation of HSC.更多还原