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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。
OBJECTIVE: To observe the effects of high dose methylprednisolone on neuronal apoptosis and neurological function after chronic compression spinal cord injury in rats. Methods: Sixty Wistar rats of the same age were placed into posterior compression device to make a moderate chronic compression spinal cord injury model. Randomly divided into high-dose methylprednisolone treatment group (A group, 30) and simple chronic spinal cord injury group (B group, 30). In situ terminal deoxynucleotidyl transferase - mediated dUTP labeling (TUNEL) technique was used to detect the apoptosis of spinal cord injury area at 1, 3, 7, 14 and 28 days after chronic compressive spinal cord injury. Results: Apoptosis was found in both A and B groups. There was significant difference between the two groups (P <0.01 and 0.05). The reduction in apoptosis in the treated group was consistent with the restoration of neurological function. Conclusion: Chronic compression spinal cord injury can lead to cell apoptosis. High dose methylprednisolone can inhibit neuronal apoptosis.