TY- JOR T1-通风诱导的有丝分裂原激活蛋白激酶途径JF的激活JF-欧洲呼吸杂志JO -EUR RESSIR J SP -946 LP -946 LP -956 DO -10.1183/09031936.02.02.01612001 VL- 20U. au -Haitsma，J.J。Au -Goldmann，T。Au -Poelma，D.L。au -lachmann，B。au -uhlig，S。y1 - 2002/10/01 ur -http：//www.qdcxjkg.com/content/20/4/946.abstract n2-患者的机械通气可以是寿命- 节省治疗，但也会对肺部施加额外的压力。有丝分裂原激活的蛋白激酶（MAPK）代表了一种蛋白激酶家族，它们被许多不同形式的胁迫磷酸化和激活。使用蛋白质印迹分析，本研究分析了高差压力通气对MAPK细胞外信号相关激酶（ERK）激活的影响-1/2，C- Jun氨基末端激酶（JNK）和p38激酶，以及P38激酶，以及在MAPK激活的转录因子C-JUN上，ETS样蛋白（ELK）-1和激活转录因子（ATF）-2。在成年大鼠中，高压通风（在CMH2O中45/10峰值的峰值压力/阳性端 - 验证压力）30或60分钟不会影响动脉氧合，但导致ERK-1/2的磷酸化增强，JNK，C，C，C，C，与正常通风（13/3）大鼠相比，Jun，Elk-1和ATF-2。ERK-1/2和JNK的激活位于类似II型肺泡细胞的细胞上。此外，高压通气增强了核因子（NF）-κB抑制剂（NF）-κB和转录因子NF-κB的核转运的磷酸化。 In isolated perfused mouse lungs, the MAPK/ERK kinase inhibitor U0126 prevented ventilation-induced activation of ERK-1/2 and Elk-1, but had no effect on ventilation-induced cytokine release. The present authors conclude that mechanical ventilation triggers specific signalling pathways, such as the mitogen-activated protein kinase and the nuclear factor-κB pathways, which may contribute to pulmonary inflammation and proliferation. This study was financially supported by the Deutsche Forschungsgemeinschaft Grant DFG Uh 88/2-4 and by the International Foundation for Clinically Oriented Research (IFCOR). ER -