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