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  • Title: P38 mitogen-activated protein kinase inhibition attenuates pulmonary inflammatory response in a rat cardiopulmonary bypass model.
    Author: Dong X, Liu Y, Du M, Wang Q, Yu CT, Fan X.
    Journal: Eur J Cardiothorac Surg; 2006 Jul; 30(1):77-84. PubMed ID: 16723252.
    Abstract:
    OBJECTIVE: Cardiopulmonary bypass (CPB) produces an inflammatory response associated with pulmonary dysfunction. P38 mitogen-activated protein kinase (P38MAPK) have been shown to mediate pulmonary inflammatory response after CPB, we examined the effect of SB203580, a specific p38 MAPK inhibitor, on CPB-induced pulmonary inflammatory response. METHODS: Sprague-Dawley rats (n=54) were randomized into three groups (each n=18): (1) S group, rats underwent sham CPB; (2) CPB group, rats underwent CPB; (3) SB group, rats underwent CPB plus pretreatment with SB203580 (10 mg/kg, i.v., 30 min before CPB). The lung samples were collected after 10 min, 60 min, and 150 min lung reperfusion (each n=6) in CPB group and SB group, and after 70 min, 120 min, and 210 min observation in S group as the control. RESULTS: The level of lung phospho-IkappaBalpha, nuclear factor (NF)-kappaB 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)-alpha and interleukin (IL)-1beta 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 expression and production, and reduced lung inflammation. CONCLUSIONS: These findings suggested that (1) p38 MAP kinase activation is one of the important aspects of the signaling event that mediate the release of TNF-alpha and IL-1beta and contributes to CPB-induced pulmonary inflammatory response, (2) SB203580 selectively inhibiting p38 MAP kinase activation efficaciously reduces pulmonary inflammatory response after CPB, and (3) p38 MAP kinase influence the activation of NF-kappaB in the lung during and after CPB.
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