P38 Mapk In Cardiopulmonary Bypass And Pulmonary Inflammatory Response In The Role Of Experimental Research

Objective: Cardiopulmonary bypass (CPB) produces an inflammatory response associated with pulmonary dysfunction.Mitogen-activated protein kinase (MAPK) have been shown to mediate pulmonary inflammatory response after CPB , we examined the change of MAPK during and after CPB and the effect of SB203580, a specific P38 MAPK inhibitor, on CPB induced pulmonary inflammatory response.Metholds: Sprague-Dawley rats (n=54) were randomized into three groups(each=18): (1) S group, rats underwent sham CPB; (2) CPB group, rats underwent CPB ; (3) SB group,rats underwent CPB puls pretreatment with SB203580 (10 mg/kg i.v, 30 hour before CPB). The lung was excised immediately after being sacrificed at 10 min,60 min,150 min lung reperfusion(each n=6) in CPB group and SB group,and after 70min , 120 min, 210 min observation in S group.ResμLts: The level of activities of JNK ,ERK, P38 MAPK in CPB group increased than S group.The level of lung phospho-ikBα, nuclear factor (NF)-kB activity and Activating Protein (AP)-1 activity in CPB group was increased than S group.CPB resulted in increased pulmonary tissue tumor necrosis factor (TNF)-α and interleukin (IL)-1β expression and production, increased pulmonary inflammatory response. The in vivo administration of SB203580 prevented up-regulation of lung phosphorylated P38 MAP kinase, decreased pulmonary tissue level of proinflammatory cytokines express and production, reduced lung inflammation.Conclusions:These findings suggested that ( 1 ) The rat model of CPB waseasy to establish and should facilitate the investigation of the pathophysiological processes concerning CPB-related pulmonary dysfunction and possible protective interventions. (2) JNK ,ERK and P38 MAPK are activitated in pulmonary tissue during and after CPB (3)P38 MAP kinase activation is one important aspect of the signaling event that mediate the release of TNF-α and IL-1β and...