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机构地区:[1]上海中医药大学附属龙华医院呼吸科,上海200032
出 处:《中国新药与临床杂志》2007年第3期161-166,共6页Chinese Journal of New Drugs and Clinical Remedies
基 金:国家中医药管理局资助项目(NO972100)
摘 要:目的:探讨止喘胶囊对哮喘大鼠气道重建TGF-β1及其胞内信号转导分子Smads蛋白的影响。方法:将40只雄性SD大鼠随机分为5组:正常对照组、哮喘模型组、止喘胶囊组、地塞米松组和止喘胶囊+地塞米松组,每组8只。通过ip卵清蛋白及右腿im氢氧化铝凝胶致敏,并雾化吸入卯清蛋白,建立哮喘模型,在哮喘激发4 wk后检测肺组织TGF-β1蛋白及mRNA以及Smad-2、Smad-7 mRNA表达。计量资料用ANOVA程序进行分析,并用LSD进行两两比较。结果:哮喘模型组气道上皮TGF-β1以及TGF-β1 mRNA表达显著高于正常对照组(P<0.05,P<0.01)。哮喘模型组Smad-2 mRNA较正常对照组表达明显升高(P<0.05),止喘胶囊组、止喘胶囊+地塞米松组和地塞米松组TGF-β1,TGF-β1 mRNA,Smad-2 mR- NA表达显著低于哮喘模型组(P<0.01或P<0.05),止喘胶囊组可显著上调Smad-7 mRNA表达水平,与哮喘模型组相比有显著的差异(P<0.05)。结论:止喘胶囊可下调哮喘大鼠生长因子TGF-β1蛋白及mR- NA、Smad-2 mRNA表达,上调Smad-7 mRNA的表达,阻断TGF-β1的信号转导,从而减轻哮喘大鼠气道重建,为止喘胶囊的临床使用提供实验依据。AIM: To evaluate the effects of Zhichuan capsule on expression of TGF-β1, Smad-2, and Smad-7 in TGF-β1 signal transduction path in airway remodeling of bronchial asthmatic rats. METHODS: The model was established by different density ovalbumin (1%, 2 %, 3 %), then sensitized and activatived in pro, longed and repeated exposure. The rats were randomly divided into normal control group, model group; Zhichuan capsule group, dexamethasone group, and Zhichuan capsule plus dexamethasone group. General histological changes were observed by hematoxylin and eosin stained sections after 4 wk activation. The expression of TGF-β1, TGF-1β mRNA, Smad-2 mRNA, Smad-7 mRNA, and the airway were examined by immunocytochemistry and RT-PCR. Statistical comparison was performed by ANOVA followed by Fisher LSD test. RESULTS: The expression of TGF-β1, TGF-β1 mRNA, and Smad-2 mRNA in model group are higher than those in nomal control group (P 〈 0.05 or P 〈 0.01). The expression of TGF-β1, TGF-β1 mRNA, and Smad-2 mRNA in Zhichuan capsule group, Zhichuan capsule plus dexamethasone group, and dexamethasone group are lower than those in model group (P 〈 0.01 or P 〈 0.05). The level of Smad-2 mRNA is higher in Zhichuan capsule group than that in dexamethasone group. CONCLUSION: Zhichuan capsule could down-regulate the expression of TGF-β1, TGF-β1 mRNA and Smad-2 mRNA, up-regulate the expression of Smad-7 mRNA, and suppress airway remodeling.
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