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目的探讨布地奈德早期干预对急性哮喘模型大鼠转化生长因子-β1(TGFβ-1)/Smad信号传导通路影响。方法30只健康雄性清洁级Wistar大鼠随机均分成正常对照组(C组)、哮喘模型组(A组)和布地奈德组(B组)等3组,每小组10只,用卵白蛋白(OVA)制备哮喘大鼠模型,通过早期布地奈德混悬液雾化吸入方式对急性哮喘模型大鼠进行干预,用双抗体夹心ELISA法测定血清和支气管肺泡灌洗液(BALF)中TGF-β1浓度,免疫组化方法检测肺组织TGF-β1以及磷酸化Smad2/3(P-Smad2/3)、Smad7蛋白表达水平。结果C组的血清、BALF中TGF-β1浓度分别低于A组和B组,B组血清、BALF中TGF-β1浓度较A组下降;A组肺组织P-Smad2/3蛋白表达较C组和B组增高,而Smad7蛋白表达下降。结论布地奈德早期干预可抑制急性哮喘大鼠体内TGFβ-1和P-Smad2/3的过度表达及上调Smad7,从而阻断TGFβ-1的胞内信号转导,可在一定程度上减轻急性哮喘大鼠气道炎症和抑制气道重塑的发生发展。
Objective To investigate the effect of early intervention of budesonide on TGFβ-1 / Smad signaling pathway in acute asthmatic rats. Methods Thirty healthy male Wistar rats were randomly divided into three groups: normal control group (group C), asthma model group (group A) and budesonide group (group B), 10 mice in each group were treated with ovalbumin OVA) to establish asthma model in rats. The asthmatic model rats were treated by inhalation of early budesonide suspension, and the levels of TGF-β1 in serum and bronchoalveolar lavage fluid (BALF) were determined by double antibody sandwich ELISA The expression of TGF-β1 and P-Smad2 / 3 and Smad7 protein in lung tissue were detected by immunohistochemistry. Results The concentrations of TGF-β1 in serum and BALF in group C were lower than those in group A and group B, respectively. The concentrations of TGF-β1 in serum and BALF in group B were lower than those in group A. The expression of P-Smad2 / 3 in group A was significantly higher than that in group C And group B increased, while Smad7 protein expression decreased. Conclusion Budesonide can inhibit the over-expression of TGFβ-1 and P-Smad2 / 3 and Smad7 in acute asthmatic rats and block the intracellular signal transduction of TGFβ-1, which can relieve the acute asthma to a certain extent Airway inflammation and inhibition of airway remodeling in rats.