【摘要】 目的探讨猪MODS时p38MAPK介导的TNF-α对内皮祖细胞(EPC)的调控作用,从EPC分化障碍的角度进一步研究创伤后MODS的发病机制。方法将20头家猪分为MODS组(M组)和对照组(C组),每组10头。采用"二次打击法"建立猪MODS模型,监测其各主要脏器功能的变化,体内用Western-blot法检测外周血单核细胞p38MAPK的磷酸化变化,用ELISA法测定外周血血浆TNF-α的浓度变化,流式细胞仪检测外周血EPC的数量变化。结果M组的MODS发生率明显高于C组,M组外周血单核细胞p38MAPK的磷酸化明显增强,TNF-α合成与分泌明显增加,外周血EPC数量与功能下降。结论外周血单核细胞p38MAPK的磷酸化使TNF-α的转录、合成增加,血浆TNF-α升高,使外周血中的EPC其数量与功能下降,炎症病理反应加重,可能是MODS的发病机制。更多还原

【Abstract】 Objective To study the modulation of EPC by p38 mitogen activated protein kinase(MAPA)mediated TNF-α and the pathogenesis in multiple organ dysfunction syndrome.Methods Twenty porcines were divided into control(C)group and MODS(M)group.After establishment of MODS model,the fumction of main organs was determined.In vivo,the p38MAPK phosphorylation in the peripheral blood mononuclear cell was monitored with Western-blot,and TNF-α mRNA measured with RT-PCR,plasma TNF-α was measured with ELISA and EPC with FCM.Results The mobidity in group M was much higher than that in group C.In vivo the peripheral monocellular p38MAPK phosphorylation was much more intense,the synthesis and secretion of TNF-α was markedly increased,and the quantity and function of EPC was markedly decreased.Conclusions The peripheral monocellular p38MAPK phosphorylation can induce TNF-α mRNA transcription and increase its synthesis,and TNF-α of the peripheral blood mononuclear cell is increased,The increased TNF-α of the peripheral blood plasma could result in decrease of the quantity and function of EPC,and aggravate the inflammatory response of MODS,which could be the pathogenesis of MODS.更多还原