目的:研究降脂颗粒对小鼠非酒精性脂肪性肝炎(NASH)的肝纤维化的作用。方法:雄性C57BL/6小鼠24只,随机分为正常、蛋氨酸-胆碱缺乏(MCD)和降脂颗粒组。正常组小鼠予普通饲料,其余两组小鼠予MCD饲料,降脂颗粒组同时予降脂颗粒灌胃。6周后,处死各组动物并取肝组织固定或冻存。观察各组小鼠肝组织天狼猩红染色结果,用ELISA方法检测血清纤溶酶原激活物抑制因子-1(PAI-1)含量,应用荧光定量RT-PCR和/或Western blot检测肝组织PAI-1、转化生长因子-β1(TGF-β1)、α-平滑肌肌动蛋白(α-SMA)及Ⅰ型胶原α1(COL1A1)表达水平。结果:MCD组的肝组织出现广泛肝细胞脂肪变性,及窦周胶原组织增加,而降脂颗粒组肝细胞周围无明显胶原沉积。MCD组小鼠血清PAI-1含量较正常组小鼠显著升高(P<0.001),与MCD组比较,降脂颗粒组PAI-1含量下调(P<0.05)。MCD组小鼠肝组织PAI-1、α-SMA、TGF-β1和COL1A1 m RNA水平均较正常组显著升高(P<0.01,P<0.001),在降脂颗粒组中这些促纤维化基因的表达下调(P<0.05)。与正常组比较,肝组织PAI-1和α-SMA蛋白表达水平在MCD组显著升高,与MCD组比较,在降脂颗粒组表达均显著下调。结论:降脂颗粒对MCD饮食诱导的小鼠NASH肝纤维化具有预防作用,其机制可能与调控NASH中肝纤维化相关因子的表达从而抑制星状细胞活化、胶原增生及促进细胞外基质降解相关。 Objective: To investigate the effect of Jiangzhi granule on hepatic fibrosis in mice with non-alcoholic steatohepatitis (NASH). Methods: Twenty - four male C57BL / 6 mice were randomly divided into normal, methionine - choline deficiency (MCD) and jiangzhi group. The normal group of mice to normal feed, the remaining two groups of mice to MCD feed, lipid-lowering particles at the same time to lipid-lowering particles gavage. After 6 weeks, the animals in each group were killed and the liver tissues were fixed or frozen. The results of Sirius red staining were observed in liver tissues of each group. The level of PAI-1 was detected by ELISA. The expression of PAI in liver tissue was detected by real-time RT-PCR and / or Western blot. -1, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA) and collagen type Ⅰ α (COL1A1) Results: The liver tissue of MCD group showed extensive hepatocellular steatosis and increased collagen in sinusoids, whereas there was no significant collagen deposition around the hepatocytes in Jiangzhi granules group. The level of PAI-1 in MCD group was significantly higher than that in normal group (P <0.001). Compared with MCD group, the level of PAI-1 in Jiangzhi group was decreased (P <0.05). The levels of PAI-1, α-SMA, TGF-β1 and COL1A1 mRNA in MCD group were significantly higher than those in normal group (P <0.01, P <0.001) (P <0.05). Compared with normal group, the expressions of PAI-1 and α-SMA in liver tissue were significantly increased in MCD group, compared with MCD group, the expression of PAI-1 and α-SMA in Jiangzhi granule group were significantly down-regulated. Conclusion: Jiangzhi Granule can prevent mice liver fibrosis induced by MCD, and its mechanism may be related to the regulation of the expression of hepatic fibrosis related factors in NASH and the inhibition of stellate cell activation, collagen hyperplasia and extracellular matrix degradation .