中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2009年
9期
518-520
,共3页
毛岸荣%黄河%方国恩%马立业%毕建威%罗天航%付文政%华积德
毛岸榮%黃河%方國恩%馬立業%畢建威%囉天航%付文政%華積德
모안영%황하%방국은%마립업%필건위%라천항%부문정%화적덕
多器官功能障碍综合征%p38丝裂素活化蛋白激酶%肿瘤坏死因子-α%磷酸化
多器官功能障礙綜閤徵%p38絲裂素活化蛋白激酶%腫瘤壞死因子-α%燐痠化
다기관공능장애종합정%p38사렬소활화단백격매%종류배사인자-α%린산화
multiple organ dysfunction syndrome%p38 mitogen activated protein kinase%tumor necrosis factor-α%phosphorylation
目的 探讨猪多器官功能障碍综合征(MODS)中p38丝裂素活化蛋白激酶(p38MAPK)磷酸化对肿瘤坏死因子-α(TNF-α)基因表达调控的影响.方法 将30头家猪随机均分为MODS组和对照组,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.采用蛋白质免疫印迹法(Western blotting)检测外周血单核细胞p38MAPK的磷酸化水平,用实时荧光定量聚合酶链反应(PCR)测定TNF-α mRNA表达,用酶联免疫吸附法(ELISA)测定血浆TNF-α浓度.结果 MODS时外周血单核细胞p38MAPK磷酸化明显增强,使TNF-α mRNA表达明显增强、血浆TNF-α浓度显著升高,与对照组比较差异均有统计学意义(P<0.05或P<0.01).结论 在MODS发病机制中,外周血单核细胞p38MAPK磷酸化使TNF-α基因的转录活性明显增强,从而使血浆TNF-α升高,这是MODS时TNF-α生成增加的机制.
目的 探討豬多器官功能障礙綜閤徵(MODS)中p38絲裂素活化蛋白激酶(p38MAPK)燐痠化對腫瘤壞死因子-α(TNF-α)基因錶達調控的影響.方法 將30頭傢豬隨機均分為MODS組和對照組,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.採用蛋白質免疫印跡法(Western blotting)檢測外週血單覈細胞p38MAPK的燐痠化水平,用實時熒光定量聚閤酶鏈反應(PCR)測定TNF-α mRNA錶達,用酶聯免疫吸附法(ELISA)測定血漿TNF-α濃度.結果 MODS時外週血單覈細胞p38MAPK燐痠化明顯增彊,使TNF-α mRNA錶達明顯增彊、血漿TNF-α濃度顯著升高,與對照組比較差異均有統計學意義(P<0.05或P<0.01).結論 在MODS髮病機製中,外週血單覈細胞p38MAPK燐痠化使TNF-α基因的轉錄活性明顯增彊,從而使血漿TNF-α升高,這是MODS時TNF-α生成增加的機製.
목적 탐토저다기관공능장애종합정(MODS)중p38사렬소활화단백격매(p38MAPK)린산화대종류배사인자-α(TNF-α)기인표체조공적영향.방법 장30두가저수궤균분위MODS조화대조조,채용실혈성휴극여내독소혈증적"이차타격법"건립저MODS모형.채용단백질면역인적법(Western blotting)검측외주혈단핵세포p38MAPK적린산화수평,용실시형광정량취합매련반응(PCR)측정TNF-α mRNA표체,용매련면역흡부법(ELISA)측정혈장TNF-α농도.결과 MODS시외주혈단핵세포p38MAPK린산화명현증강,사TNF-α mRNA표체명현증강、혈장TNF-α농도현저승고,여대조조비교차이균유통계학의의(P<0.05혹P<0.01).결론 재MODS발병궤제중,외주혈단핵세포p38MAPK린산화사TNF-α기인적전록활성명현증강,종이사혈장TNF-α승고,저시MODS시TNF-α생성증가적궤제.
Objective To investigate that the phosphorylation of the p38 rnitogen activated protein kinase (p38MAPK) influences gene expression of tumor necrosis faetor-α (TNF-α) in multiple organ dysfunction syndrome (MODS) in pigs. Methods Thirty pigs were divided into MODS group and control group, and an animal model of MODS of "two-hit" injury, including hemorrhagic shock and endotoxemia, was reproduced. The content of p38MAPK's phosphorylation was assessed with Western blotting. TNF-α mRNA in peripheral blood monocytes was assayed with real time-polymerase chain reaction (RT-PCR). TNF-α was monitored in the peripheral blood plasma with enzyme linked immunosorbent assay (ELISA). Results Phosphorylation of p38MAPK was obviously increased in extent, which enhanced gene expression of TNF-α and then secretion of TNF-α by the peripheral blood mononuelear cell in MODS, and the differenees were statistically significant compared with that of control group (P<0.05 or P<0.01). Conclusion p38MAPK's phosphorylation is important in pathogenesis of MODS, and phosphorylation of p38MAPK ean enhance TNF-α mRNA transcription and secretion of TNF-α from peripheral blood mononuelear cells, which is the mechanism of increased TNF-α in MODS.
