摘要
Abstract
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,high-dose 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.关键词
右美托咪定/磷脂酰肌醇3-激酶/蛋白激酶B/核因子E2相关因子2信号通路/胸部创伤/肺组织损伤Key words
dexmedetomidine/PI3K/Akt/Nrf2 signaling pathway/thoracic trauma/lung tissue injury分类
医药卫生
