表没食子儿茶素没食子酸酯对酒精性肝病小鼠肝脏Tf和TfR1表达的影响

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目的:探讨表没食子儿茶素没食子酸酯(EGCG)对酒精性肝病(ALD)小鼠肝脏转铁蛋白(Tf)、转铁蛋白受体1(TfR1)表达的影响。方法:6~8周龄雄性无特定病原体(SPF)级C57/BL6小鼠随机分为正常组和模型组,模型组小鼠每日予乙醇灌胃,并于造模第9周随机分为模型组,EGCG 10,20,30 mg·kg-1组。给药4周后处死小鼠,观察各组小鼠肝脏病理变化,并测定肝功能、肝肝铁含量,采用蛋白免疫印迹法检测肝组织Tf,TfR1的表达。结果:模型组小鼠与正常对照组相比血清谷丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平显著升高(P<0.01),肝组织病理表现肝细胞呈中度脂肪变性,肝铁含量及肝脏Tf,TfR1表达显著升高(P<0.01)。EGCG治疗组显著降低血清ALT,AST水平(P<0.01),肝组织病理变化可见显著改善,肝铁含量及肝脏Tf,TfR1表达显著降低(P<0.01)。结论:EGCG可以降低ALD小鼠肝脏Tf,TfR1的表达水平,抑制肝铁摄取,从而发挥其对酒精性肝病的保护作用。 Objective: To investigate the effect of epigallocatechin gallate (EGCG) on the expression of hepatic transferrin (Tf) and transferrin receptor 1 (TfR1) in mice with alcoholic liver disease (ALD). Methods: Six to eight weeks old male SPF-free C57 / BL6 mice were randomly divided into normal group and model group. The mice in model group were given intragastric administration of ethanol daily and were randomly divided into Model group, EGCG 10,20,30 mg · kg-1 group. Four weeks after the administration, the mice were sacrificed and the pathological changes of the liver in each group were observed. The liver function and liver-liver iron content were measured. The expression of Tf and TfR1 in the liver tissue were detected by Western blotting. Results: The levels of ALT and AST in model group were significantly higher than those in normal control group (P <0.01). The pathological changes of liver tissue in model group were moderately fatty Degeneration, liver iron content and liver Tf, TfR1 expression was significantly increased (P <0.01). The levels of ALT and AST in serum in the EGCG treatment group were significantly lower than those in the control group (P <0.01). The histopathological changes in the liver tissue were significantly improved. The content of hepatic iron and the expression of Tf and TfR1 in the liver were significantly decreased (P <0.01). CONCLUSION: EGCG can reduce the expression of Tf and TfR1 in the liver of ALD mice and inhibit the hepatic iron uptake, thus exerting its protective effect on alcoholic liver disease.
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