To investigate the role of miR-128-3p and MAPK14 in the dexmedetomidine treatment of acute lung injury in septic mice. SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO₂, PaCO₂, MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to detect the targeting relationship of miR-128-3p and MAPK14, and qPCR and WB were used to detect the expression of miR-128-3p and MAPK14. Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased (all p < 0.05). Compared with the Model group, the contents of MDA, MPO, inflammatory factors in the DEX group and miR-128-3p mimic group were significantly decreased, and the content SOD was significantly increased, however, opposite results were occurred in oe-MAPK14 group (all p < 0.05). Compared with the DEX group, all the indicators in miR-128-3p mimic+DEX group showed significant improvement (all p < 0.05). Compared with the miR-128-3p mimic group, all the indicators were deteriorated in the miR-128-3p mimic+oe-MAPK14 group (all p < 0.05). The combination of DEX and oe-MAPK14 blocked the protective effect of dexmedetomidine on acute lung injury in septic mice. miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

目的探讨miR-128-3p和MAPK14在右美托咪定治疗脓毒症小鼠急性肺损伤中的作用。SPF C57BL / 6小鼠分为8组。观察肺组织的病理变化，湿重/干重比（W / D），PaO ₂，PaCO ₂，MDA，SOD和MPO水平以及血清炎症因子水平。用双重荧光素酶报告基因检测法检测miR-128-3p和MAPK14的靶向关系，用qPCR和WB检测miR-128-3p和MAPK14的表达。与正常组相比，其他各组的MDA，MPO，炎性因子水平和MAPK14的表达水平较低，而SOD的含量和miR-128-3p的表达水平则显着降低（所有p <0.05）。与模型组相比，DEX组和miR-128-3p模拟组的MDA，MPO，炎性因子含量明显降低，SOD含量显着增加，但是oe-MAPK14组却出现了相反的结果（所有p  <0.05）。与DEX组相比，miR-128-3p mimic + DEX组的所有指标均表现出显着改善（均p  <0.05）。与miR-128-3p模拟组相比，miR-128-3p模拟+ oe-MAPK14组的所有指标均下降（所有p <0.05）。DEX和oe-MAPK14的组合阻断了右美托咪定对败血症小鼠急性肺损伤的保护作用。miR-128-3p可以通过靶向和抑制MAPK14的表达来进一步增强右美托咪定对败血症小鼠急性肺损伤的保护作用。