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目的:探讨壳聚糖介导的CrmA对小鼠肝纤维化的治疗效果,以期为肝纤维化的基因治疗提供实验基础。方法:清洁级的75只雄性小鼠随机分为正常组、模型组、壳聚糖介导的CrmA组、壳聚糖介导的空载体组、壳聚糖组,每组15只。应用30%四氯化碳橄榄油溶液3 ml/kg腹腔注射制备肝纤维化小鼠模型。治疗8周后,眼眶取血,检测血清的肝功能指标,并取肝组织做HE染色,观察各组小鼠肝脏的病理形态,Real Time PCR检测肝组织IL-1β、α-SMA、TGF-β1、TIMP-1表达量。结果:与模型组小鼠相比,壳聚糖介导的CrmA组小鼠的肝纤维化程度减轻,ALT、AST显著降低(P<0.01),肝组织IL-1β、α-SMA、TIMP1、TGF-β1的表达明显减少(P<0.05),而模型组、壳聚糖介导的空载体组和壳聚糖组均无显著性差异。结论:壳聚糖介导的CrmA能有效减轻肝纤维化小鼠的肝脏损伤和纤维化程度,为基因治疗肝纤维化提供了一种潜在的新思路和方法。
Objective: To investigate the therapeutic effect of chitosan-mediated CrmA on liver fibrosis in mice, in order to provide experimental basis for gene therapy of liver fibrosis. Methods: Seventy-five male mice were randomly divided into normal group, model group, chitosan-mediated CrmA group, chitosan-mediated empty vector group and chitosan group, 15 rats in each group. Hepatic fibrosis mouse model was established by intraperitoneal injection of 30% carbon tetrachloride olive oil solution 3 ml / kg. After 8 weeks of treatment, the orbital blood was collected to detect the serum liver function indexes. The liver tissues were harvested for HE staining. The pathological changes of the liver of each group were observed. The expression of IL-1β, α-SMA and TGF- β1, TIMP-1 expression levels. Results: Compared with the model group, the chitosan-mediated CrmA group reduced the degree of hepatic fibrosis, the ALT and AST were significantly decreased (P <0.01), and the levels of IL-1β, α-SMA, TIMP1, The expression of TGF-β1 was significantly decreased (P <0.05), but there was no significant difference between model group and chitosan-mediated empty vector group and chitosan group. CONCLUSION: Chitosan-mediated CrmA can effectively reduce liver injury and fibrosis in mice with hepatic fibrosis and provide a potential new idea and method for gene therapy of hepatic fibrosis.