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目的:探讨三叶香茶菜防治大鼠肝纤维化的作用机制。方法:大鼠每3 d接受一次背部sc 40%CCl4花生油(首次5 mL·kg-1,其余为3 mL·kg-1),连续8周引发肝纤维化模型,造模同时每日分别给予三叶香茶菜提取物20,40,80 g·kg-1灌胃。给药8周后取血,ELISA法测定大鼠血清中Ⅲ型前胶原(proeollagen typeⅢ,PCIII)、透明质酸(hyaluronic acid,HA)、金属蛋白酶组织抑制因子-1(tissue inhibitor of metalloproteinase-1,TIMP-1)、基质金属蛋白酶-2(matrix metal oproteinase-2,MMP-2)及肝脏中转化生长因子-β1(transforming growth Factor-β1,TGF-β1)含量;Masson染色病理切片观察肝脏胶原纤维生成。结果:模型组血清中HA,PCIII,TGF-1及TIMP-1含量较正常组显著升高(P<0.01),且MMP-2浓度显著下降(P<0.01)。与模型组比较,三叶香茶菜高、中剂量组能显著降低大鼠血清HA,PCIII,TIMP-1的含量,提高MMP-2含量(P<0.01);并能显著降低肝组织TGF-β1水平(P<0.01)。三叶香茶菜低剂量组能显著降低大鼠血清HA,PCIII含量(P<0.05);并有降低血清TIMP-1及肝组织TGF-β1水平,提高MMP-2含量的趋势。结论:三叶香茶菜能有效减轻慢性肝损伤大鼠肝纤维化程度,其作用机制可能与调节TGF-β1水平,控制肝星状细胞释放TIMP-1及MMP-2有关。
Objective: To investigate the mechanism of clover tea in prevention and treatment of hepatic fibrosis in rats. METHODS: Rats were given sc 40% CCl4 peanut oil (first 5 mL · kg-1, the rest being 3 mL · kg-1) every 3 days for 4 weeks. Liver fibrosis models were induced for 8 weeks. Clover tea tea extract 20,40,80 g · kg-1 orally. The blood samples were taken for 8 weeks and the serum levels of proeollagen type Ⅲ (PCIII), hyaluronic acid (HA), tissue inhibitor of metalloproteinase-1 , TIMP-1, MMP-2 and transforming growth factor-β1 (TGF-β1) in the liver were observed. Masson staining was used to observe the contents of collagen Fiber generation. Results: The contents of HA, PCIII, TGF-1 and TIMP-1 in model group were significantly higher than those in normal group (P <0.01), and the concentration of MMP-2 was significantly decreased (P <0.01). Compared with the model group, high and medium doses of clover Chard could significantly reduce the levels of serum HA, PCIII and TIMP-1 and increase the content of MMP-2 (P <0.01), and significantly decrease the expression of TGF- β1 level (P <0.01). The low dose of clover Chard low dose group could significantly reduce the content of serum HA and PCIII (P <0.05), decrease the level of serum TIMP-1 and TGF-β1 of liver tissue and increase the content of MMP-2. Conclusion: clover tea can effectively reduce the degree of hepatic fibrosis in rats with chronic liver injury. The mechanism may be related to the regulation of TGF-β1 and the release of TIMP-1 and MMP-2 by hepatic stellate cells.