目的 观察中药复方金三莪抗大鼠肝纤维化的疗效及其机制。方法 将 5 0只 Wistar大鼠随机分为 4组 :A组为正常组 (n=8),B组为肝纤维化模型组 (n=14 ),C组为金三莪治疗低剂量组 (n=14 ),D组为金三莪治疗高剂量组 (n=14 )。B,C,D组大鼠 sc CCl4 诱导大鼠肝纤维化模型,C,D组大鼠于造模第 4周开始 ig金三莪,剂量分别为 0.6,1.2 g/10 0 g,每日 1次 ;A,B组 ig生理盐水 1ml/kg,第 8周处死全部大鼠。免疫组化技术检测转化生长因子 - β1 (TGF- β1 ),Smad3及 Sm ad7在肝内的表达及定位 ;常规生化方法检测肝功能 ;放射免疫方法检测透明质酸 (HA )含量 ;Van Gieson染色和 HE染色观察肝组织病理形态学改变。结果 肝纤维化模型大鼠经金三莪治疗后肝组织内 TGF- β1 及 Smad3表达降低,而 Sm ad7的表达增加,与模型组大鼠比较差异显著 (P<0.0 5 ),TGF- β1 及Sm ad3的免疫阳性反应信号主要位于纤维间隔中的细胞浆,Smad7则主要在肝细胞浆表达。与模型组比较,金三莪治疗后大鼠血清丙氨酸氨基转移酶 (AL T),天门冬氨酸氨基转移酶 (AST),HA含量显著减低 (P<0.0 5 ) ;肝小叶结构趋于正常,纤维间隔明显变薄 (P<0.0 1)。结论 中药复方金三莪能有效减轻肝纤维化大鼠的肝脏损伤及纤维化程度,其机制与抑制.

Object To investigate the therapeutic effects and mechanism of traditional Chinese compound decoction of Radix Curcumae (RC),Rhizoma Sparganii (RS), and Rhizoma Zedoariae (RZ) (DRRR) on liver fibrosis in rat sinduced by carbon tetrachloride ( CCl₄).Methods Fifty Wistar rats were randomly divided into four groups: group A was healthy control (n= 8),group B was model rats of liver fibrosis induced by CCl₄ (n=14), group C and D were treated with DRRR after the liver fibrosis in rats induced by CCl₄ four weeks later (n=14).B, C, and D groups were injected subcutaneo usly with CCl₄ ; C and D groups were administ rated with DRRR 0.6 and 1.2g/100g, once perday. A fter administration of DRRR four weeks all rats were sacrificed, their blood and liver were harvested for further examination.The effect of DRRR was explored by the expressions and sites of transforming growth factor-beta1 (TGF-β), Smad3 and Smad7 in liver tissues by immunohistochemical staining. The liver function, serum hyaluronic acid (HA), and liver histopathology were also examined by biochemsitry, RIA, HE, and Van Gieson stainings respect ively. Results To compare with model group, in rats that received DRRR, the expressions of TGF-β and Smad3 were significantly decreased, while the expression of Smad7 was obviously increased in the livers (P<0.05),the levels of serum ALT and AST were markedly decreased, HA content ( P<0.05) was considerably attenuated and liver fibrosis as assessed by histology ( P<0.01).Conclusion The DRRR has protective effects on liver injury and can inhibit liver fibrosis in rats induced by CCl₄. The mechanisms possibly contribute to it saction of anti-inf lammatory, which is relative to its effect of down-regulating TGF-β and Smad3, up-regulating Smad7 and results in suppressing the activation of hepatic stellate cells.

湖北省教育厅基金资助项目 (2003X113)