黄芪甲甙对实验性肺纤维化大鼠Cathepsin B表达的影响

目的:探讨黄芪甲甙时实验性肺纤维化大鼠肺组织中组织蛋白酶B(Cathepsin B,CB)表达的影响。方法:36只SD大鼠,随机分为对照组、模型组和干预组。模型组和干预组气管内注射博来霉素(BLM,5mg/kg)诱导肺纤维化,对照组在相同条件下给予生理盐水。第二天起干预组大鼠每天经胃管灌服0．1g/L黄芪甲甙2ml,其余两组相同条件下给予助溶剂羧甲基纤维素钠。治疗的第7d和28d,处死动物取出肺组织,进行病理学观察;测定28d肺组织中羟脯氨酸含量;用免疫组化和RT-PCR观察各组鼠肺组织CB蛋白及mRNA表达的水平。结果:病理学观察显示:与模型组比较,干预组肺泡炎和纤维化程度均减轻;模型组羟脯氨酸含量显著增高,而干预组与模型组比较羟脯氨酸含量明显降低;与模型组比较,干预组CB蛋白及mRNA表达显著降低。结论:黄芪甲甙可能通过押制CB的过度表达,对实验性大鼠肺纤维化具有良好的治疗作用。

Effect of Astragalaside on Cathepsin B Expression in the Lung of Rats with Experimental Pulmonary Fibrosis

Objective:To investigate the effect of Astragalaside on Cathepsin B expression in the lungs of rats with experimental pulmonary fibrosis.Methods:Thirty-six Spague-Dawley rats were randomly divided into the control group,model Group and treatment group.The model group and the treatment group were induced to produce pulmonary fibrosis with bleomycin endotracheally,while the control group was given normal saline in the same condition.From the second day the rats in the treatment group were treated with 0.1g/L astragaloside 2 ml ig,while the other two groups of rats,with CMC 2ml intragastric injection instead.On the seventh day and the twenty-eighth day the Lungs were isolated.Pathological changes in the lungs were evaluated by HE stain and Masson's trichrome stain.The hydroxyprolline of pulmonary homogenate were measured for evaluation of the degree of pulmonary fibrosis.The mRNA expression of CB was evaluated by RT-PCR quantitative analysis,and the immunohistochemical method was used to investigate the change of CB protein.Results:The degree of alveolitis and pulmonary fibrosis in treatment group was improved compared with that of model group.Compared with control group,the hydroxyprolline was obviously increased in model group,but compared with model group,the hydroxyprolline was obviously decreased in treatmeat group.The expression level of GB and mRNA in treatment group was significantly decreased compared with model group.Conclusion:Aswagalaside might play pivotal role in curing the experimental pulmonary fibrosis in Spague-Dawley rats by suppressing excessive expressing of lung CB.