Objective: To investigate the mechanism by which dexmedetomidine (DEX) improves lung tissue injury
in rats with thoracic trauma by regulating the PI3K/Akt/Nrf2 signaling pathway. Methods: Male Sprague Dawley rats
were randomly grouped into control group, model group, low-dose DEX (DEX-L, 10 μg · kg-1 · d-1 DEX) group, highdose
DEX (DEX-H, 50 μg · kg-1 · d-1 DEX) group, and high-dose DEX+LY294002 (DEX-H+LY, 50 μg · kg-1 · d-1
DEX+5 mg · kg-1 · d-1 PI3K inhibitor LY294002) group. The ratio method was applied to determine the lung index
of rats. The wet/dry weight ratio of the lungs was measured. ELISA was used to measure the inflammatory factor
levels in rat bronchoalveolar lavage fluid. H-E staining was applied to determine pulmonary histopathology. Western
blotting was applied to determine the expression of PI3K/Akt/Nrf2 pathway proteins. Results: Compared with
the control group, the lung tissue of the model group rats showed inflammatory infiltration, loose arrangement,
and thickening of alveolar walls, with the lung index, lung wet/dry weight ratio, levels of IL-1β, IL-6, TNF-α in
bronchoalveolar lavage fluid, and inflammation score increased, while the expression of PI3K, Akt, and Nrf2 proteins
decreased. Compared with the model group, the DEX-L and DEX-H groups showed reduced lung tissue injury in
rats, with the lung index, lung wet/dry weight ratio, levels of IL-1β, IL-6, TNF-α in bronchoalveolar lavage fluid, and
inflammation score decreased, while the expression of PI3K, Akt, and Nrf2 increased. Compared with the DEX-H
group, the lung tissue injury in the DEX-H+LY group worsened, with the lung index, lung wet/dry weight ratio, levels
of IL-1β, IL-6, TNF-α in bronchoalveolar lavage fluid, and inflammation score increased, while the expression of
PI3K, Akt, and Nrf2 decreased. Conclusion: DEX may
improve lung tissue injury in rats with thoracic trauma
by activating the PI3K/Akt/Nrf2 signaling pathway
