Protective Effects Of Dexmedetomidine On Spinal Cord After Ischemia-reperfusion Injury In Rats

Objective: To observe the protective effects of dexmedetomidine on spinal cord after ischemia-reperfusion(IR)injury in rats and to find out its possible mechanism.Methods: 30 male rats were randomly divided into three groups,which were sham operation group,untreated group and dexmedetomidine group.The rat spinal cord ischemic/reperfusion injury model was established by Zivin method.The hindlimb motor function was scored at 6 h,12 h,24 h and 48 h after reperfusion.Scoring Criteria: Rat Motor Nerve Functional Rating Rat hind limb motor function was assessed according to the Behrmann(1993)5-point grading method.48 hours after ischemia-reperfusion,the anterior lumbar vertebral gray matter at L5 site was measured and anti-P-AKT polyclonal antibody was used to perform immunohistochemical staining.The expression level of P-AKT in each experimental group was evaluated using a scoring scale.The score criteria were 0(no expression),1(positive),2(strong positive).The expression of P-AKT in the anterior horn of ischemic reperfusion was detected.The apoptotic index of reperfusion neurons in the spinal cord was detected in situ using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL).The neuronal nuclear staining was yellow or brown yellow,which was positive,and the apoptosis index(AI)was used as the evaluation standard.The apoptotic index refers to the percentage of apoptotic cells that appear in at least 1000 cells in each section of spinal cord tissue.Results:The hind-limb motor function was normal in the sham operation group.The rats in the untreated group and the dexmedetomidine group had different degrees of spasticity after ischemia-reperfusion.The recovery of hindlimb motor function in the dexmedetomidine group was better than that in the untreated group,and dexmedetomidine could significantly improve the hindlimb motor function of the rat after spinal cord ischemia/reperfusion injury(P<0.05)..The expression of P-AKT in dexmedetomidine group was significantly higher than that in sham operation group and untreated group.Dexmedetomidine increased theexpression of P-AKT in the anterior horn of spinal cord(P<0.05).No obvious neuronal apoptosis was found in the sham group.A large number of apoptotic neurons were observed in the spinal cord of the untreated group.Apoptotic neurons in the dexmedetomidine group were significantly less than those in the untreated group,and dexmedetomidine could inhibit the apoptosis of spinal cord neurons induced by ischemia/reperfusion injury(P<0.05).Conclusion:The protective effects of dexmedetomidine against spinal cord injury induced by IR may be related to activation of PI3K/Akt pathway,thus inhibit the neuronal apoptosis.