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目的:探讨福尔肝6号抗肝纤维化的作用机理。方法:采用二甲基亚硝胺(DMN)腹腔注射诱导大鼠肝纤维化模型,以福尔肝6号灌胃治疗,每日1次,共4周,并以γ-干扰素(γ-IFN)为治疗对照。肝组织病理检查与丽春红胶原染色,检测大鼠血清生化肝功能,肝组织超氧化物歧化酶(SOD)活性,丙二醛(MDA)与羟脯氨酸(Hyp)含量变化,进行 Hyp、MDA 与 SOD 之间的相关分析。结果:模型大鼠肝组织胶原明显增加,纤维间隔形成;血清 ALT 水平上升;肝组织 SOD 活性明显下降,MDA 与 Hyp 含量明显升高,且 MDA与 Hyp 含量呈正相关,SOD 与 Hyp 含量呈负相关。福尔肝6号与γ-IFN 均能明显减轻肝组织胶原沉积,显著降低血清 ALT 水平,提高肝组织 SOD 活性,降低 MDA 与 Hyp 含量,两药物组间无明显差别。结论:DMN可引起肝脏脂质过氧化,DMN 肝纤维化与脂质过氧化密切相关;福尔肝6号有良好抗肝脂质过氧化作用,该作用为福尔肝6号治疗肝纤维化的重要作用机理。
Objective: To investigate the mechanism of anti-hepatic fibrosis in Fuergan 6. METHODS: Rat hepatic fibrosis model induced by intraperitoneal injection of dimethylnitrosamine (DMN) was treated with Fuergan 6 once daily for 4 weeks with γ-interferon (γ- IFN) was the treatment control. Liver histopathological examination and Ponceau collagen staining, detection of serum biochemical liver function, liver superoxide dismutase (SOD) activity, malondialdehyde (MDA) and hydroxyproline (Hyp) content, Hyp , correlation analysis between MDA and SOD. RESULTS: Compared with the Hyp content, SOD was negatively correlated with the increase of collagen in liver tissue and the formation of fibrous septa, the increase of serum ALT level, the decrease of SOD activity in liver tissue, the increase of MDA and Hyp content, and the positive correlation between MDA and Hyp content. . Both Folg-6 and γ-IFN significantly reduced collagen deposition in liver tissue, significantly reduced serum ALT levels, increased liver SOD activity, and decreased MDA and Hyp levels. There was no significant difference between the two drug groups. Conclusion: DMN can induce hepatic lipid peroxidation, DMN hepatic fibrosis is closely related to lipid peroxidation, and Forg-6 has good anti-hepatic lipid peroxidation. This effect is Fuergan 6 in treating liver fibrosis. The important mechanism of action.