摘要目的 观察大鼠脊髓缺血再灌注损伤后应用钙蛋白酶特异性抑制剂E-64-D,对脊髓神经细胞组织学改变和凋亡的影响及对大鼠后肢运动功能的保护作用.方法 选用纯种雄性成年SD大鼠106只,夹闭右肾动脉分支下腹主动脉30 min,再灌注即刻静脉应用钙蛋白酶特异性抑制剂E-64-D,观察再灌注后3、24、72 h和7 d脊髓损伤节段神经细胞的凋亡及再灌注后24、72h组织病理学改变;对再灌注后72 h的大鼠后肢功能进行评分.结果 脊髓缺血再灌注24 h开始出现神经细胞凋亡现象,脊髓组织出现病理学改变,神经元死亡,胶质细胞增生.应用E-64-D后,凋亡现象和细胞坏死得到抑制,差异有统计学意义(P<0.01).再灌注后72 h后肢功能也得到一定程度的保护.结论 脊髓再灌注损伤后静脉应用E-64-D治疗,可以明显抑制脊髓神经细胞的凋亡,有利于神经元的存活,损伤后3 d大鼠后肢运动功能得到一定程度的改善.

abstractsObjective To observe the effects of Ca]pain-specific inhibitor E-64-D on the apoptesis and pathohistological change of neural cells in rat spinal cord after ischemia-reperfusion injury and the neu-roprotective effects on the motor function of hind-limb after 72 h of reperfusion. Methods The abdominal aortas of male Sprague-Dawley (SD) rats were clipped for 30 min and intravenously treated with E-64-D. After reperfussion for 3 h, 24 h, 72 h or 7 days, the apeptosis and pathohistological changes of neural cells were observed. The motor function score of hind-limb after 72 h of reperfusion was recorded. Results The apoptosis and pathohistological changes of neural cells were found after 24 h of reperfnsion in the spinal cord sections. The intravenous treatment of E-64-D could significantly protect the spinal cord after reperfu-sion. After 72 h of reperfusion, the motor function of hind-limp in the treated group had a higher function score than the ischemia-reperfusion group. Conclusion Post-injury intravenous treatment of E-64-D can inhibit the apoptosis and pathohistological changes of neural cells in the spinal cord sections after ischemia-reperfusion injury, favor the survival of neurons, and improve the motor function of the hind-limp in rats af-ter 72 h of injury to some extent.