中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2009年
6期
603-606
,共4页
毛岸荣%方国恩%周虹%马立业%毕建威%罗天航%付文政%华积德
毛岸榮%方國恩%週虹%馬立業%畢建威%囉天航%付文政%華積德
모안영%방국은%주홍%마립업%필건위%라천항%부문정%화적덕
多器官功能障碍综合征%p38丝裂原活化蛋白激酶%IL-1β%内皮祖细胞%体内
多器官功能障礙綜閤徵%p38絲裂原活化蛋白激酶%IL-1β%內皮祖細胞%體內
다기관공능장애종합정%p38사렬원활화단백격매%IL-1β%내피조세포%체내
Multiple organ dysfunction syndrome%p38 mitogen activated protein kinase%Interleukin-1β%En-dothelial progenitor cell%In vivo
目的 探讨猪多器官功能障碍综合征(MODS)中p38MAPK介导的白介素(IL)～1β对内皮祖细胞(EPC)的数量与功能的调控,从血管内皮祖细胞分化障碍来研究创伤后MODS的发病机制.方法 将30头家猪随机分为MODS组(n=15,M组)、对照组(n=15,C组),采用失血性休克与内毒素血症的"二次打击法"建立猪MODS模型,在体内Western-blot法检测外周血单核细胞p38MAPK的磷酸化变化;ELISA法测定外周血血浆IL-1β的浓度变化;流式细胞仪检测外周血EPC数量的变化;采用x2检验比较M组与C组的MODS发生率,采用成组t检验比较M组与C组的p38MAPK的磷酸化变化、外周血血浆IL-1β的浓度变化与外周血EPC数量的变化.结果 在MODS中外周血单核细胞p38MAPK的磷酸化增强,导致其外周血IL-1β浓度升高,从而使得外周血EPC数量下降,M组MODS的发生率均明显高于C组(P<0.01);M组的外周血单核细胞p38MAPK的磷酸化与外周血血浆IL-1β的浓度明显高于C组(P<0.01);M组外周血EPC数量明显低于C组(P<0.01).结论 在猪MODS的发病机制中,外周血单核细胞内的p38MAPK的磷酸化使血浆IL-1β浓度升高,使EPC的数量下降,致使MODS的炎症反应加重.
目的 探討豬多器官功能障礙綜閤徵(MODS)中p38MAPK介導的白介素(IL)～1β對內皮祖細胞(EPC)的數量與功能的調控,從血管內皮祖細胞分化障礙來研究創傷後MODS的髮病機製.方法 將30頭傢豬隨機分為MODS組(n=15,M組)、對照組(n=15,C組),採用失血性休剋與內毒素血癥的"二次打擊法"建立豬MODS模型,在體內Western-blot法檢測外週血單覈細胞p38MAPK的燐痠化變化;ELISA法測定外週血血漿IL-1β的濃度變化;流式細胞儀檢測外週血EPC數量的變化;採用x2檢驗比較M組與C組的MODS髮生率,採用成組t檢驗比較M組與C組的p38MAPK的燐痠化變化、外週血血漿IL-1β的濃度變化與外週血EPC數量的變化.結果 在MODS中外週血單覈細胞p38MAPK的燐痠化增彊,導緻其外週血IL-1β濃度升高,從而使得外週血EPC數量下降,M組MODS的髮生率均明顯高于C組(P<0.01);M組的外週血單覈細胞p38MAPK的燐痠化與外週血血漿IL-1β的濃度明顯高于C組(P<0.01);M組外週血EPC數量明顯低于C組(P<0.01).結論 在豬MODS的髮病機製中,外週血單覈細胞內的p38MAPK的燐痠化使血漿IL-1β濃度升高,使EPC的數量下降,緻使MODS的炎癥反應加重.
목적 탐토저다기관공능장애종합정(MODS)중p38MAPK개도적백개소(IL)～1β대내피조세포(EPC)적수량여공능적조공,종혈관내피조세포분화장애래연구창상후MODS적발병궤제.방법 장30두가저수궤분위MODS조(n=15,M조)、대조조(n=15,C조),채용실혈성휴극여내독소혈증적"이차타격법"건립저MODS모형,재체내Western-blot법검측외주혈단핵세포p38MAPK적린산화변화;ELISA법측정외주혈혈장IL-1β적농도변화;류식세포의검측외주혈EPC수량적변화;채용x2검험비교M조여C조적MODS발생솔,채용성조t검험비교M조여C조적p38MAPK적린산화변화、외주혈혈장IL-1β적농도변화여외주혈EPC수량적변화.결과 재MODS중외주혈단핵세포p38MAPK적린산화증강,도치기외주혈IL-1β농도승고,종이사득외주혈EPC수량하강,M조MODS적발생솔균명현고우C조(P<0.01);M조적외주혈단핵세포p38MAPK적린산화여외주혈혈장IL-1β적농도명현고우C조(P<0.01);M조외주혈EPC수량명현저우C조(P<0.01).결론 재저MODS적발병궤제중,외주혈단핵세포내적p38MAPK적린산화사혈장IL-1β농도승고,사EPC적수량하강,치사MODS적염증반응가중.
Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.
