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目的:探讨肝康乐抗二甲基亚硝胺(DMN)诱导大鼠肝纤维化的作用及机制。方法:将72只Wistar大鼠随机分成6组,每组12只,分别为:正常对照组、模型组、水飞蓟素阳性对照组及肝康乐高、中、低剂量组,采用DMN腹腔注射制备肝纤维化大鼠模型,给药6周后观察各组大鼠肝功能、肝纤维化指标、肝组织病理学、肝组织脂质过氧化水平及肝纤维化相关蛋白表达的变化。结果:模型组肝组织呈现典型的肝纤维化改变,与正常对照组比较,模型组大鼠血清ALT、AST、TBil、HA、LN、PCⅢ、CollagenⅣ水平及肝组织Hyp、MDA含量显著升高,血清Alb水平及肝组织SOD、GSH-Px活性显著降低,肝组织α-SMA、CollagenⅠ、MMP2和TGF-β_1蛋白表达水平显著升高。与模型组比较,肝康乐高、中剂量组肝纤维化病理学改变明显减轻,血清ALT、AST、TBil、HA、LN、PCⅢ、CollagenⅣ水平及肝组织Hyp、MDA含量显著降低,肝组织SOD、GSH-Px活性显著升高,肝组织α-SMA、CollagenⅠ、MMP2和TGF-β_1蛋白表达水平显著降低。结论:肝康乐能显著减轻DMN诱导的大鼠肝纤维化水平,其作用机制可能与抑制氧化应激和TGF-β_1表达有关。
Objective: To investigate the effect and mechanism of liver and Kangle anti-dimethylnitrosamine (DMN) -induced liver fibrosis in rats. Methods: Seventy-two Wistar rats were randomly divided into 6 groups with 12 rats in each group: normal control group, model group, silymarin-positive control group and Hepang Lok high, medium and low dose groups. DMN was injected intraperitoneally After 6 weeks of administration, the changes of hepatic function, hepatic fibrosis indexes, liver histopathology, liver lipid peroxidation and hepatic fibrosis related protein expression were observed. Results: Compared with the normal control group, the levels of serum ALT, AST, TBil, HA, LN, PCⅢ, Collagen Ⅳ and Hyp, MDA in liver tissue of the model group were significantly increased, Serum Alb levels and liver SOD, GSH-Px activity decreased significantly, liver α-SMA, Collagen Ⅰ, MMP2 and TGF-β 1 protein levels were significantly increased. Compared with the model group, the pathological changes of hepatic fibrosis in high and middle dose of liver and liver were significantly reduced, the level of serum ALT, AST, TBil, HA, LN, PCⅢ, Collagen Ⅳ and Hyp, MDA in liver tissue were significantly decreased, GSH-Px activity was significantly increased, liver α-SMA, Collagen Ⅰ, MMP2 and TGF-β 1 protein levels were significantly reduced. Conclusion: Hekangle can significantly reduce the level of hepatic fibrosis induced by DMN in rats, which may be related to the inhibition of oxidative stress and TGF-β 1 expression.