黄芪多糖对肺纤维化大鼠细胞因子及肺组织病理结构的影响  

Effects of Astragalus Polysaccharides on Level of Cytokines and Pathological Structure of Lung Tissue in Rat Model of Pulmoanry Fibrosis

作　　者：李娟[1] 张毅[1] 刘永琦[1] 李金田[1] 魏舒畅[1] 苏韫[1] 聂蕾[1] 

机构地区：[1]甘肃中医学院,甘肃兰州730000

出　　处：《时珍国医国药》2011年第7期1684-1685,共2页Lishizhen Medicine and Materia Medica Research

基　　金：国家教育部春晖计划基金资助项目(No.Z2004-1-620039)

摘　　要：目的观察肺纤维化大鼠血清中IFN-γ、IL-4、TNF-α的含量、肺组织病理结构变化,进一步探讨黄芪多糖干预治疗肺纤维化的作用机理。方法 Wistar大鼠60只随机分为5组:空白组、博莱霉素(BLM)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复制肺纤维化模型,造模后第2天开始各药物组开始干预治疗,14d采用酶联免疫吸附法测定血清IFN-γ、IL-4、TNF-α的含量,14 d、28 d采用HE染色观察肺组织病理结构的变化。结果与空白组相比较,BLM组大鼠血清IFN-γ含量降低,IL-4、TNF-α的含量升高(均P<0.05),肺组织的肺泡炎及纤维化程度升高(均P<0.05);与BLM组比较,黄芪多糖组、黄芪水提物组、地塞米松组大鼠血清IFN-γ含量升高,IL-4、TNF-α含量降低(均P<0.05);肺组织的肺泡炎及纤维化程度降低(P<0.05)。结论应用黄芪多糖可以明显减轻大鼠肺纤维化进程,不仅降低Ⅱ型细胞因子(IL-4)含量,而且升高Ⅰ型细胞因子(IFN-γ)及TNF-α含量,从而调整Ⅰ型/Ⅱ型细胞因子平衡及及TNF-α表达达到抗纤维化作用。ObjectiveTo observe the effect of Astragalus polysaccharides on the levels of IFN-γ、IL-4 and TNF-α in serum and pathological structure of lung tissue in BLM-induced pulmonary fibrosis rats.MethodsSixty wistar rats were divided randomly into normal,model,Astragalus decoction and Astragalus polysaccharide groups.Pulmonary fibrosis model was established by injection of Bleomycin（BLM） via trachea（5mg/kg）.After 24h,rats were given drugs by ig in all groups once daily.On d14 and d28,6 rats were killed and the lungs were collected for observing pathological structure of lung tissue by HE staining.Interleukin-4（IL-4）,interferon gamma（IFN-γ） and Tumor necrosis factor-α（TNF-α） in serum were detected by enzyme linked immunosorbent assay（ELISA）.ResultsCompared with normal group,IFN-γ content was significantly lowered,while IL-4 and TNF-α were considerably increased in model group（P〈0.05）;compared with model group,IFN-γ content was significantly elevated（P〈0.05）,IL-4,TNF-α levels were significantly decreased（P〈0.05）.The degree of fibrosis was alleviated in Astragalus decoction and Astragalus polysaccharide groups（P〈0.05）.ConclusionAstragalus polysaccharides tain protective effect by regulating pulmonary fibrosis in rat Ⅰ/Ⅱ type cytokines balance and TNF-α level,thereby interfering with the occurrence of pulmonary interstitial fibrosis and development.

关 键 词：肺纤维化 黄芪多糖 细胞因子 病理结构 

分 类 号：R285.5[医药卫生—中药学]