右美托咪啶对脂多糖所致急性肺损伤小鼠的保护作用

The protective effect of dexmedetomidine on acute lung injury induced by lipopolysaccharide

目的探讨右美托咪啶(DEX)对脂多糖(LPS)诱导的急性肺损伤(ALI)小鼠是否有保护作用。方法实验小鼠按随机数字表法分为三组,LPS组(腹腔注射LPS)、LPS+DEX组1(腹腔注射LPS+50μg/kg DEX)、LPS+DEX组2(腹腔注射LPS+25μg/kg DEX),每组6只,HE染色观察各组肺组织光镜病理改变;全自动生化仪测量C-反应蛋白;Western blot方法测凋亡蛋白Caspase-3表达。结果 HE染色显示LPS组肺间质充血、水肿,大量炎性细胞浸润,两种剂量DEX干预组可明显改善肺组织病理变化;与LPS组相比,两种剂量的DEX干预组C-反应蛋白水平及凋亡蛋白Caspase-3的表达明显减少(P <0.05)。结论右美托咪啶能够减轻LPS诱导的AL1小鼠肺组织炎症反应及凋亡蛋白的表达。

Objective To investigate whether dexmedetomidine （Dex） has a protective effect a- gainst acute lung injury （ALI） in lipopolysaccharide （LPS） induced mice model. Methods Mice were randomly allocated into three groups as follows： LPS group （LPS administration） , LPS ＋ Dex groupl （LPS administration ＋50μg/kg Dex）, and LPS ＋ Dex group2 （LPS administration ＋ 25 μg/kg Dex）. Lung tissue sections were stained with hematoxylin and eosin （HE） to observe the pathological changes. The c-reactive protein was measured with automatic biochemical analyzer. The apoptotic marker Caspase-3 expression was detected by Western blot. Results HE staining showed pulmonary interstitial congestion, edema and inflammatory cell infiltration in LPS group. Intraperitoneal injection of dexmedetomidine could significantly improve the pathological changes of lung tissue. Compared with LPS group, C-reactive protein and Caspase- 3 were significantly reduced in dexmetomidine group. Conclusions Dexmedetomidine attenuates LPS-in- duced inflammatory reaction and apoptosis in mice.