急性呼吸窘迫综合征大鼠血小板丝裂原活化蛋白激酶p38磷酸化水平

Determination of Platelet Mitogen-activated Protein Kinase p38 Phosphorylation Levels in Rats with ARDS

目的研究ARDS发病时血小板激活的信号传导途径。方法将SD大鼠30只分为5组,其中4组制作油酸型ARDS模型(经尾静脉注射油酸0.25 mL/kg),1组为对照组(注射等体积生理盐水)。注油酸后2、6、24、72 h或盐水后2 h,从腹主动脉收集血液以分离血小板,提取血小板蛋白,用免疫印迹法检测血小板丝裂原活化蛋白激酶p38(p38 MAPK)的磷酸化水平。将其与肺病理变化情况进行比较分析。结果 2～72 h ARDS模型组血小板内p38 MAPK磷酸化的水平均高于对照组,以2 h组为最高,变化规律与肺病理变化情况大体一致。结论 MAPKs信号转导通路的启动可能参与了ARDS的发病。

Objective To study the signal transduction pathway for platelet activation at the onset of ARDS.Methods Thirty SD rats were divided into five groups.Four groups were made oleic acid-type ARDS models(0.25 ml/kg oleic acid via tail vein injection).One group was as control group(injection of an equal volume of normal saline).Blood was collected from abdominal aorta to separate platelets after 2,6,24,and 72 hours after oleic acid injection or 2 hours after saline.Platelet protein was extracted and the platelet mitogen-activated protein kinase p38(p38 MAPK)phosphorylation level was detected by immunoblotting.Compare it with lung pathological changes.Results The levels of p38 MAPK phosphorylation in platelets were significantly higher in the ARDS model group than in the control group at 2 to 72 hours.The 2h group was the highest.The changes were generally consistent with the lung pathological changes.Conclusion The initiation of MAPKs signal transduction pathway may be involved in the pathogenesis of ARDS.