【摘要】 目的:观察大剂量甲基强的松龙对大鼠慢性压迫性脊髓损伤后神经细胞凋亡及神经功能恢复的影响。方法:将60只同龄Wistar大鼠,置入后路渐进式压迫装置,制作成中度慢性压迫性脊髓损伤模型。随机分为大剂量甲基强的松龙治疗组(A组,30只)和单纯慢性压迫性脊髓损伤组(B组,30只)。应用原位末端脱氧核糖核苷酸转移酶介导dUTP标记(TUNEL)技术,分别于慢性压迫性脊髓损伤后1、3、7、14、28d对脊髓损伤区进行细胞凋亡检测。结果:A、B两组均发现细胞凋亡,两组细胞凋亡率比较,差异有显著性(P<0.01和0.05)。治疗组细胞凋亡的减少与神经功能的恢复相一致。结论:慢性压迫性脊髓损伤可导致细胞凋亡,大剂量甲基强的松龙对神经细胞凋亡可起到抑制作用。更多还原

【Abstract】 Objective: To explore the effect of high dose methylprednisolone(MP) on cell apoptosis after chronic compressive spinal cord injury in rat.Method:60 Wistar rats were divided equally into 2 groups, chronic compressive spinal cord injury(CCSCI) and high dose methylprednisolone group(Group A) and chronic compressive spinal cord injury group(Group B).The cell apoptosis of spinal slice from spinal cord injured by the chronic compression was examined by the terminal deoxynucleotidal transferase-mediated DUTP-biotin nick end labeling(TUNEL) reaction, and the neurological function was measured in 1,3,7,14 and 28 days post-operatively. The positive cells were quantitated by a computer image analysis system.Result:Positive expression of apoptotic cell appeared both in Group A and Group B.There were significant statistic difference remained between Group A and Group B(P<0.01 and 0.05).The decrease of cell apoptosis was paralleled by a significant improvement in neurological function evaluated by open-field and inclined plane tests.Conclusion:Chronic compressive spinal cord injury can induced apoptosis, high dose methylprednisolone can inhabit apoptosis after CCSCI.更多还原