中文摘要：

目的研究黄芪多糖对博莱霉素（BLM）所致肺纤维化大鼠模型血清中Th1／Th2细胞因子平衡、一氧化氮（NO）含量的影响，探讨黄芪阻抑肺纤维化的效应及其机制。方法Wistar大鼠随机分为对照组、模型组、地塞米松组、黄芪水提物组、黄芪多糖组，每组12只。采用气管内一次性注入BLM复制肺纤维化大鼠模型，造模后第2天开始药物干预治疗，14、28d各取6只大鼠，分别检测血清中干扰素γ（IFN-γ）、白介素（IL）-4和NO水平。结果与对照组比较，模型组大鼠IFN-γ水平、IFN-γ／IL-4比值明显降低，IL4和NO的含量明显升高（P〈0．01）；与模型组比较，黄苠多糖组、黄芪水提物组、地塞米松组大鼠IFN-γ水平、IFN-γ／IL-4比值明显升高，除黄芪多糖14d组外余各组NO水平明显降低（P〈0．05，P〈0．01）；黄芪多糖组、黄芪水提物组与地塞米松组比较，各指标均差异不显著（P〉0．05）。结论黄芪多糖对肺纤维化大鼠肺组织均具有保护作用，调节Th1／Th2型细胞因子的平衡及NO代谢可能是其阻抑肺纤维化发生的机制之一。

英文摘要：

Objective To observe the effects of astragalus polysaccharides on the balance of T helperl/T helper2 （Th1/Th2） cytokines and the level of nitric oxide （NO） in Bleomycin （BLM） -induced pulmonary fibrosis rats, and to explore its underlying mechanisms. Methods Wistar rats were randomly divided into control, model, Dexamethasone, astragalus decoction and astragalus polysaccharides groups. Pulmonary fibrosis models were established by injection of BLM via trachea （5 mg/kg）. After 24 h, rats were given drugs once daily. At 14 and 28 d, 6 rats of each group were killed for detecting the levels of interleukin-4 （IL-4） ,interferon gamma （ IFN-3,） ,NO in the serum. Results In comparison with those in control group, the levels of IFN-γ/and the ratio of IFN-γ/IL-4 were significantly decreased, while the levels of IL-4 and NO were increased and the degree of fibrosis was higher in model group （P 〈0. 01） ;whereas compared with those in model group, the levels of IFN-5, and the ratio of IFN-γ/IL-4 were significantly increased（ P 〈 0. 05, P 〈 0.01 ） , except to astragalus polysaccharities group of 14 d, the level of NO was significantly lower in dexamethasone, astragalus decoction and astragalus polysaccharides groups （ P 〈 0. 05, P 〈 0. 01 ）. No significant differences were found between astragalus polysaccharides group, Astragalus decoction group and dexamethasone group in these indexes （P 〉 0. 05 ）. Conclusions Astragalus polysaccharides has the protective effect on the process of pulmonary fibrosis rats. Its mechanisms maybe relate to balancing cytokine, regulating the metabolism of nitric oxide.