右美托咪定在大鼠脊髓缺血再灌注损伤中的 保护作用及机制研究

目的 探讨右美托咪定对大鼠脊髓缺血/再灌注损伤的保护作用及PI3K/Akt传导通路在其中的作用。方法 30只成年雄性大鼠随机分为假手术组、模型组和右美托咪定治疗组，每组10只。建立大鼠脊髓缺血/再灌注损伤模型,对再灌注损伤后6 h、12 h、24 h、48 h实验大鼠后肢运动功能进行评分，检测缺血脊髓前角组织中P-AKT的表达水平及神经元的凋亡指数。结果 右美托咪定可改善脊髓缺血/再灌注损伤后实验大鼠的后肢运动功能(P＜0.05)；提高脊髓前角P-AKT的表达水平(P＜0.05)，抑制缺血/再灌注损伤所致的脊髓神经元的凋亡(P＜0.05)。结论 右美托咪定对脊髓缺血/再灌注损伤有一定的保护作用，其机制可能与激活PI3K/Akt传导通路，从而抑制神经元的凋亡有关。

Protective Effects and Mechanism of Dexmedetomidine on Spinal Cord Ischemia-Reperfusion Injury in Rats

Abstract:Objective To investigate the protective effect of dexmetomidine on spinal cord ischemia/reperfusion injury in rats and the role of PI3K/Akt pathway in it.Methods 30 adult male rats were randomly divided into the sham operation group,the model group and the right metomomidine treatment group,with 10 rats in each group.A rat model of spinal cord ischemia/reperfusion injury was established.The hindlimb motor function was scored at 6 h,12 h,24 h,and 48 h after reperfusion,and the expression of P-AKT in the anterior horn of ischemic spinal cord was detected.Levels and neuronal apoptosis index.Results Dexmedetomidine can improve the hindlimb motor function in rats after spinal cord ischemia/reperfusion injury(P<0.05),increase the expression level of P-AKT in the anterior horn of spinal cord(P<0.05),and inhibit the apoptosis of spinal cord neurons induced by ischemia/reperfusion(P<0.05). Conclusion Dexmedetomidine has a protective effect on spinal cord ischemia/reperfusion injury,and its mechanism may be related to activation of PI3K/Akt conduction pathway and inhibition of neuronal apoptosis.