止喘胶囊对哮喘大鼠气道重建的TGF-β1及Smads蛋白表达的影响

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。

Effects of Zhichuan capsule on expression of TGF-β1, Smad-2, and Smad-7 in bronchial asthmatic rats with airway remodeling

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-β1 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 expres- sion 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-β1mRNA,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 dex- amethasone 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.