ARDS大鼠血小板细胞外调节的蛋白激酶磷酸化水平变化
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摘要
目的探讨丝裂原活化蛋白激酶(MAPKs)信号转导通路与急性呼吸窘迫综合征(ARDS)发病的关系。方法 30只健康大鼠随机分为5组。实验组4组,经尾静脉注射油酸制做ARDS动物模型(0.25 mL/kg);对照组1组注射等量生理盐水。注射油酸后2、6、24、72 h或盐水后2 h,从腹主动脉取血分离血小板,提取血小板蛋白,用免疫印迹法检测血小板细胞外调节的蛋白激酶(ERK)的磷酸化水平。将ERK磷酸化水平与肺病理变化情况进行比较分析。结果 2～24 h实验组动物血小板内ERK磷酸化的水平高于对照组,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 ARDS时有MAPKs信号转导通路的启动;ARDS的发病可能与MAPKs信号转导通路启动有关。
Objective To explore the relationship between mitogen-activated protein kinase(MAPKs) signal transduction pathway and the pathogenesis of acute respiratory distress syndrome(ARDS). Methods Thirty healthy rats were randomLy divided into 5 groups.4 groups as experimental group, ARDS animal models were prepared by tail vein injection of oleic acid 0.25 m L/kg. 1 group as control group, an equal volume of saline was injected. At 2h, 6h, 24 h, and 72 h after oleic acid injection, 2h after saline injection, blood was taken from the abdominal aorta. Platelets were isolated, platelet proteins were extracted, and the level of phosphorylation of extracellularlyregulated protein kinase(ERK) in platelets was detected by Western blotting. ERK phosphorylation levels were compared with lung pathological changes. Results The platelet ERK phosphorylation levels in 2-24 h experimental group were higher than those in control group, Peaked at 2h, then decreased gradually(P<0.05). The change pattern is generally consistent with the pathological changes of the lungs. Conclusion MAPKs signal transduction pathway was initiated in ARDS. The onset of ARDS may be related to the initiation of MAPKs signal transduction pathways.
Objective To explore the relationship between mitogen-activated protein kinase(MAPKs) signal transduction pathway and the pathogenesis of acute respiratory distress syndrome(ARDS). Methods Thirty healthy rats were randomLy divided into 5 groups.4 groups as experimental group, ARDS animal models were prepared by tail vein injection of oleic acid 0.25 m L/kg. 1 group as control group, an equal volume of saline was injected. At 2h, 6h, 24 h, and 72 h after oleic acid injection, 2h after saline injection, blood was taken from the abdominal aorta. Platelets were isolated, platelet proteins were extracted, and the level of phosphorylation of extracellularlyregulated protein kinase(ERK) in platelets was detected by Western blotting. ERK phosphorylation levels were compared with lung pathological changes. Results The platelet ERK phosphorylation levels in 2-24 h experimental group were higher than those in control group, Peaked at 2h, then decreased gradually(P<0.05). The change pattern is generally consistent with the pathological changes of the lungs. Conclusion MAPKs signal transduction pathway was initiated in ARDS. The onset of ARDS may be related to the initiation of MAPKs signal transduction pathways.
引文
[1]Rivera J,Lozano M L,Navarro-Nú?ez L,et al. Platelet receptors and signaling in the dynamics of thrombus formation[J]. Haematologica,2009,94(5):700-711.
[2]Rondina M T, Weyrich A S, Zimmerman G A. Platelets as Cellular Effectors of Inflammation in Vascular Diseases[J]. Circ Res,2013,112(11):1506-1519.
[3]Jenne C N, Wong C H Y, Petri B, et al. The Use of Spinning-Disk Confocal Microscopy for the Intravital Analysis of Platelet Dynamics in Response to Systemic and Local Inflammation[J]. PLoS One,2011,6(9):e25109.
[4]Stokes K Y, Granger D N. Platelets:a critical link between inflammation and microvascular dysfunction[J]. J Physiol, 2012, 590(5):1023-1034.
[5]Li C L, Li J, Li Y, et al. Crosstalk between Platelets and the Immune System:Old Systems with New Discoveries[J]. Adv Hematol,2012:384685. Published online Sep 12, 2012. doi:10.1155/2012/384685.
[6]Ware J,Corken A,Khetpal R. Platelet function beyond hemostasis and thrombosis[J]. Curr Opin Hematol,2013,20(5):10.
[7]Cooke C R,Kahn J M,Caldwell E,et al. Predictors of hospital mortality in a population-based cohort of patients with acute lung injury[J]. Crit Care Med,2008,36(5):1412-1420.
[8]Brown L M,Calfee C S,Matthay M A,et al. A simple classification model for hospital mortality in patients with acute lung injury managed with lung protective ventilation[J]. Crit Care Med,2011,39(12):2645-2651.
[9]孙辉明,施毅,宋勇,等.抗凝血酶Ⅲ对油酸诱导急性肺损伤大鼠的肺保护作用[J].中国呼吸与危重监护杂志,2011,10(2):148-153.
[10]秦开秀,王勇,简华刚.内毒素性急性肺损伤小鼠肺组织中P38MAPK的表达[J].重庆医学,2013, 42(12):1362-1364.
[11]郝佩琪,安输,杨洋,等. MEK激酶及其抑制剂的研究进展[J].中国细胞生物学学报,2015,37(10):1425-1431.
[12]刘宏,范晓枝,田新强,等. ARDS大鼠血小板MEK1磷酸化水平变化研究[J].山西大同大学学报(自然科学版),2016, 32(5):46-48.
[2]Rondina M T, Weyrich A S, Zimmerman G A. Platelets as Cellular Effectors of Inflammation in Vascular Diseases[J]. Circ Res,2013,112(11):1506-1519.
[3]Jenne C N, Wong C H Y, Petri B, et al. The Use of Spinning-Disk Confocal Microscopy for the Intravital Analysis of Platelet Dynamics in Response to Systemic and Local Inflammation[J]. PLoS One,2011,6(9):e25109.
[4]Stokes K Y, Granger D N. Platelets:a critical link between inflammation and microvascular dysfunction[J]. J Physiol, 2012, 590(5):1023-1034.
[5]Li C L, Li J, Li Y, et al. Crosstalk between Platelets and the Immune System:Old Systems with New Discoveries[J]. Adv Hematol,2012:384685. Published online Sep 12, 2012. doi:10.1155/2012/384685.
[6]Ware J,Corken A,Khetpal R. Platelet function beyond hemostasis and thrombosis[J]. Curr Opin Hematol,2013,20(5):10.
[7]Cooke C R,Kahn J M,Caldwell E,et al. Predictors of hospital mortality in a population-based cohort of patients with acute lung injury[J]. Crit Care Med,2008,36(5):1412-1420.
[8]Brown L M,Calfee C S,Matthay M A,et al. A simple classification model for hospital mortality in patients with acute lung injury managed with lung protective ventilation[J]. Crit Care Med,2011,39(12):2645-2651.
[9]孙辉明,施毅,宋勇,等.抗凝血酶Ⅲ对油酸诱导急性肺损伤大鼠的肺保护作用[J].中国呼吸与危重监护杂志,2011,10(2):148-153.
[10]秦开秀,王勇,简华刚.内毒素性急性肺损伤小鼠肺组织中P38MAPK的表达[J].重庆医学,2013, 42(12):1362-1364.
[11]郝佩琪,安输,杨洋,等. MEK激酶及其抑制剂的研究进展[J].中国细胞生物学学报,2015,37(10):1425-1431.
[12]刘宏,范晓枝,田新强,等. ARDS大鼠血小板MEK1磷酸化水平变化研究[J].山西大同大学学报(自然科学版),2016, 32(5):46-48.