摘要目的 通过观察青蒿琥酯对支气管哮喘 (简称哮喘)大鼠气道重塑的影响,并探讨其作用与TGF-β1-smad2/3信号通路的关系.方法 采用卵白蛋白激发和雾化吸入的方式建立哮喘模型,并给予药物治疗.观察各组大鼠肺组织的病理形态改变并用 Image-Pro plus 6.0图像分析软件测量大鼠支气管壁厚度和平滑肌厚度;用免疫组织化学法检测大鼠肺组织 smad2/3表达情况,RT-PCR法检测大鼠肺组织TGF-β1、smad2、smad3表达情况;ELISA法检测大鼠血清及 BALF中 TGF-β1的表达情况.结果 青蒿琥酯干预哮喘组大鼠支气管壁厚度、平滑肌厚度均明显低于哮喘组大鼠,差异有统计学意义 (P<0.01).青蒿琥酯干预哮喘组大鼠肺组织 TGF-β1、smad2、smad3 mRNA 的表达均明显低于哮喘组,差异有统计学意义 (P<0.01).青蒿琥酯干预哮喘组大鼠肺组织 smad2/smad3蛋白表达、血清及BALF中TGF-β1的表达水平均明显低于哮喘组,差异有统计学意义 (P<0.01).结论 青蒿琥酯改善哮喘大鼠气道重塑的机制可能与抑制TGF-β1-smad2/3信号通路活性有关.

abstractsObjective By observing the effect of artesunate(ART) on airway remodeling in asthmatic rats,and to investigate its relationship with TGF-β1-smad2/3 signaling pathway.Methods Clean level 32 male SD rats were randomly divided into control group,asthma group,dexamethasone group,ART group,8 rats in each group,and the way of using excitation atomization inhalation asthma model was established,and treated with drug.To observe the pathological changes of lung tissue of rats in each group,and using Image-Pro plus 6 image analysis software to measure the thickness of bronchial wall and smooth muscle thickness.The expression of smad2/3 in rat lung tissue was detected by immunohistochemistry method,the expression of TGF-β1,smad2 and smad3 in rat lung tissue was detected by RT-PCR method,the expression of TGF-β1 in serum and bronchoalveolar lavage fluid(BALF) was detected by ELISA method.Results The bronchial wall thickness and smooth muscle thickness in ART intervention group were significantly lower than those in asthma group,the difference was statistically significant(P <0.01).The expression of TGF-β1,smad2,mRNA smad3 in lung tissue of ART intervention group was significantly lower than that in asthma group,the difference was statistically significant(P<0.01).The expression of smad2/smad3 protein and TGF-β1 in serum and BALF in ART intervention group were significantly lower than those in asthma group,and the difference was statistically significant(P<0.01).Conclusions The mechanism of ART to improve airway remodeling in asthmatic rats may be related to the inhibition of TGF-β1-smad2/3 signaling pathway activity.