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.