摘要
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。
ABSTRACT：OBJECTIVE To discuss the effect of early intervention of budesonide on expressions of TGF-β1/ Smad in rats with acute asthma. METHODS Thirty Wistar rats were randomly divided into 3 groups： control group（group C）, asthma model group（group A）and budesonide therapy group（group B）, with 10 rats in each group.The model of asthma was established by the ovalbumin （OVA） challenge methods and the group B was received early therapy by inhaling budesonide. The concentration of TGF-β1 in BALF and serum were detected by ELISA. The expression of TGF-β1, phosphorylated Smad2/3（P-Smad2/3） and Smad7 proteins in lung tissue were detected by immunocytochemical method. RESULTS In BAI.F or serum, the concentration of TGF-β1 in group C was lower than that in group A or group B respectively. The concentrations of TGF-β1 in BAI.F or serum in group B was lower than that in group A.The expressions of P-Smad2/3 of group A in lung tissue was higher than that in the other two group respectively. The expressions of Smad7 of group A in lung tissue was the lowest in the three group.CONCLUSION The early intervention of budesonide could decrease the expression of TGF-β1 and P-Smad2/3, while increase the expression of Smad7 in rats with acute asthma.
出处
《海峡药学》
2012年第11期42-44,共3页
Strait Pharmaceutical Journal
