ARDS大鼠血小板MEK1磷酸化水平变化研究  被引量:2

Study on the Changes of Platelet MEk1 Phosphorylation Levels in Acute Respiratory Distress Syndrome Rats

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作  者:刘宏[1] 范晓枝 田新强[1] 李冰[1] 

机构地区:[1]山西大同大学呼吸病与职业病研究所,山西大同037009 [2]临汾市第四人民医院呼吸科,山西临汾041000

出  处:《山西大同大学学报(自然科学版)》2016年第5期46-48,共3页Journal of Shanxi Datong University(Natural Science Edition)

基  金:山西省自然科学基金资助项目[2013011055-5];大同市基础研究项目[2014105-2]

摘  要:目的探讨急性呼吸窘迫综合征(ARDS)时血小板活化的信号通路。方法 30只健康大鼠随机分为5组。实验组4组,尾静脉注射油酸(0.25ml/kg)制备ARDS模型;对照组1组,尾静脉注射等量生理盐水。注射油酸后2,6,24,72 h,注射生理盐水后2 h,从腹主动脉采血,分离血小板,提取血小板蛋白,用Western blotting技术检测血小板内丝裂原活化蛋白激酶(MAPKs)信号通路上的主要蛋白激酶之一丝裂原活化的细胞外信号调节激酶1(MEK1)的磷酸化水平变化,探讨ARDS时血小板MAPKs信号转导通路的改变及其与ARDS发病的关系。结果6~72 h实验组动物血小板内MEK1磷酸化水平明显增高,在72 h表达量最高(P〈0.05)。结论 ARDS时血小板发生了活化;其活化过程与MEK1-ERK1/2信号转导通路启动有关。Objective To investigate the signal pathway of platelet activation in acute respiratory distress syndrome(ARDS).Methods 30 healthy rats were randomly divided into 5 groups. 4 groups of them were as the experimental group, which were made ARDS rat models by intravenous injection of oleic acid(OA, 0.25ml/kg). 1 of 5 groups was as control group, was injected normal saline(NS)in same dose by intravenous. After injection of oleic acid 2 h, 6h, 24 h, 72 h, saline 2h, drawing off blood from the abdominal aorta; separating platelets; extractting platelet protein; detecting platelet mitogen-activated extracellular signal-regulated kinase 1(MEK1)phosphorylation levels by Western blotting method, which is one of major protein kinases in the mitogen-activated protein kinases(MAPKs)signal pathway, to explore the changes of platelet MAPKs signal transduction pathway in ARDS, and the relationship between the changes and the pathogenesis of ARDS. Results Platelet MEK1 phosphorylation levels were significantly increased in 6 ~ 72 h experimental animals; the highest expression at 72h(P〈0.05). Conclusion Platelet activation occurs in ARDS; the activation process of platelets are related with MEK1-ERK1/2 signaling pathway.

关 键 词:急性呼吸窘迫综合症 血小板活化 丝裂原活化蛋白激酶 信号转导 丝裂原活化的细胞外信号调节激酶1 

分 类 号:R563.8[医药卫生—呼吸系统]

 

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