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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。
Objective To investigate the regulatory effect of p38MAPK-mediated TNF-α on endothelial progenitor cells (EPCs) in porcine MODS and further study the pathogenesis of posttraumatic MODS from the perspective of EPC differentiation. Methods Twenty domestic pigs were divided into MODS group (M group) and control group (C group), with 10 in each group. The MODS model of pig was established by “second strike” to monitor the changes of the function of major organs. The phosphorylation of p38MAPK in peripheral blood mononuclear cells was detected by Western-blot in vivo, and the levels of TNF -α concentration changes, flow cytometry to detect changes in the number of peripheral blood EPC. Results The incidence of MODS in M group was significantly higher than that in C group. The phosphorylation of p38MAPK in peripheral blood mononuclear cells of M group was significantly increased, the synthesis and secretion of TNF-α were significantly increased, and the number and function of EPC in peripheral blood were decreased. Conclusion The phosphorylation of p38 MAPK in peripheral blood mononuclear cells increases the transcription and synthesis of TNF-α, and increases the level of TNF-α in plasma, which leads to the decrease of the number and function of EPC in peripheral blood and the inflammatory pathological reaction, which may be the pathogenesis of MODS .