缺氧促使鼠气道平滑肌细胞丝裂原活化蛋白酶表达

Hypoxia prompt protein expression of mitogen activated protein kinase in rat airway smooth muscle

目的探讨缺氧情况下鼠气道平滑肌细胞丝裂原活化蛋白激酶(mitogenactivatedproteinkinase,MAPK)的变化。方法雄性Wistar大鼠采用缺氧方法,用随机数字表法随机分为正常对照组、缺氧4周组,每组6只。按实验要求完成缺氧时间,12h内留取肺叶组织,行免疫组织化学。结果免疫组织化学染色显示,对照组大鼠肺小动脉内膜有散在免疫阳性染色,低氧组大鼠肺气道内膜则可见明显的免疫阳性染色。经灰度扫描,低氧组大鼠肺气道壁MAPK免疫染色阳性强度较对照组明显增强(P<0.01)。结论MAPK在缺氧性肺病引起的气道平滑肌细胞增生中可能起着重要作用。

[Objective] To explor to change of the protein expression of Mitogen activated protein kinase in rat airway smooth muscle. [Method] 12 wistar rat were divided random into normoxia group and hypoxia group, in four weeks mitogen activated protein kinase in rat airway smooth muscle were detected by immunehemistry. [Result] Mitogen activated protein kinase in rat airway smooth muscle of normoxia group was weakly stained by immunoeytochemistry, whereas the hypoxia group was strongly stained （P 〈0.01）. [Conclusions] The results suggested hypoxia prompt the protein expression of mitogen activated protein kinase in rat airway smooth muscle, which played an important role in rat airway structureal remodeling.