中文摘要：

目的：研究黄芪多糖对博莱霉素（BLM）所致肺纤维化大鼠超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）及肺上皮细胞超微结构的影响,探索黄芪阻抑肺纤维化的效应机制。方法：Wistar大鼠随机分为空白组、模型组、地塞米松组、黄芪多糖组、黄芪水提物组;采用气管内注入BLM制作大鼠肺纤维化模型,造模后第2d开始药物干预,14、28d各取6只大鼠,分别检测肺组织SOD、MDA水平,血清NO的含量,透射电镜观察肺上皮细胞超微结构变化情况。结果：与空白组比较,模型组大鼠SOD含量降低,MDA、NO的含量明显升高（均P〈0.05）;与模型组比较,黄芪多糖28d组、黄芪水提物组、地塞米松组大鼠SOD含量明显升高,NO、MDA含量明显降低（均P〈0.05）;超微结构观察,模型组肺泡Ⅱ型上皮细胞数量减少,细胞微绒毛稀少,核不规则,核染色质凝集粗块状,板层小体减少空泡样变,线粒体明显肿胀,肺泡间隔明显,纤维细胞增生明显,胞质内胶原纤维增多;各治疗组均可改善肺泡Ⅱ型上皮细胞超微结构的异常改变。结论：黄芪多糖对肺纤维化大鼠肺泡Ⅱ型上皮细胞超微结构具有保护作用,调节NO代谢,提高抗氧化能力可能是其阻抑晚期肺纤维化发生的机制之一。

英文摘要：

Objective： To observe the effect of astragalus polysaccharides on balance of levels of nitric oxide（NO）,superoxide dismutase（SOD） and malondialdehyde（MDA）,the ultrastructure in BLM-induced pulmonary fibrosis rats,and to explore its underlying mechanism.Methods： Wistar rats were randomized into control,model,Astragalus decoction and Astragalus saponins groups.Pulmonary fibrosis model was established by injection of Bleomycin（BLM）.After 24h,rats were given drugs by ig for all groups once daily.At the 14d and 28d,6 rats were killed for detecting the levels of NO in the serum,and the changes of SOD,MDA in the lung tissue.The lungs were collected for observing the ultrastructure.Results： In comparison with blank control group,the levels of SOD were significantly lower,while NO,MDA considerably higher in model group（P〈0.05）;whereas compared with model group,the levels of SOD were significantly higher（P〈0.05）,NO and MDA levels significantly lower,the degree of fibrosis was more mitigative in Astragalus decoction and Astragalus saponins（P〈0.05）.The degree of fibrosis was more mitigative by ultrastructure in Astragalus polysaccharides.Conclusion： Astragalus polysaccharides had the inhibitory effect on the process of pulmonary fibrosis.Its mechanisms maybe relate to regulating the metabolism of nitric oxide oxidative free radical.