Effects of Dexmedetomidine on Inflammatory Factors and Mitogen Activated Protein Kinase-Related Signaling Pathways of Alveolar Lavage Fluid in Mice with Lipopolysaccharide-Induced Acute Lung Injury

To investigate the effects and mechanisms of Dexmedetomidine on inflammatory factors mitogenactivated protein kinase related signaling pathways in alveolar lavage fluid mice with acute lung injury induced by lipopolysaccharide. 36 clean-grade male Kunming were randomly divided into blank control group (normal group), lipopolysaccharide-induced model group, lipopolysaccharide+dexmedetomidine 12 each group. The lipopolysaccharide intraperitoneally injected 0.1 ml 5 mg kg-1 Lipopolysaccharide, lipopolysaccharide+Dexmedetomidine 25 μg kg-1. 1 h later Lipopolysaccharide normal saline same volume as All sacrificed after intraperitoneal injection for 6 h, their tissues separated thoracotomy bronchoalveolar was recovered subsequent detection. Analysis groups tissue pathology, compare pathology score, wet weight/dry weight (W)/(D), mitogen-activated (p38 lightning, extracellular signal regulating kinase, c-jun amino terminal kinase) expression level tumor necrosis factor alpha beta, interleukin-1β, myeloperoxidase, concentration. In structure basically intact. had obvious damage, cells appeared alveoli, significantly increased exudation red blood proteins. Lipopolysaccharide+Dexmedetomidine damage improved, cell infiltration decreased, cell, decreased. Lung histopathological scores levels alpha, interleukin- 1β myeloperoxidase higher than those (p<0.05). lower concentration W/D that Protein P-P38 THE There no significant difference p38 (p>0.05). can alleviate mice, its mechanism may be realized blocking activation kinaserelated pathway thereby reducing response, providing a new target treatment sepsis futurey.