作者: Su Liu , Guang Feng , Guang-lei Wang , Gong-jian Liu
DOI: 10.1016/J.EJPHAR.2008.02.009
关键词: NF-κB 、 Pharmacology 、 Cytokine 、 Immunology 、 Respiratory disease 、 Signal transduction 、 Medicine 、 ARDS 、 Lipopolysaccharide 、 Lung injury 、 Pathogenesis
摘要: The pathogenesis of acute lung injury/acute respiratory distress syndrome (ARDS) is complex and involves multiple signal transduction processes. It believed that p38MAPK (mitogen-activated protein kinase) one the most kinases in inflammatory signaling. At present study, we demonstrated role lipopolysaccharide (LPS)-induced injury with pharmacologic inhibition by SB203580. SB203580, specific inhibitor, was injected (10 mg/kg, i.v.) 30 min before LPS administration (5 i.v.). hematoxylin-eosin staining tissues showed significantly attenuated pulmonary responses induced LPS. Moreover, SB203580 can also inhibit cytokine release, reduce mortality rate LPS-induced injury. Further, western blot analysis activation NF-kappaB, which associated IkappaBalpha degradation cytoplasm. These data suggest signaling may be involved mechanisms