大鼠脊髓损伤中的细胞凋亡及甲基强的松龙的干预作用

目的：探讨脊髓损伤（SCI）继发损伤机制，研究损伤脊髓细胞的凋亡及其意义，观察甲基强的松龙（MP）对细胞凋亡的影响。方法：使用改良Allen法制作大鼠急性SCI模型，实验分3组，假损伤（脊髓未受打击），损伤组及MP治疗组，采用HE，荧光Hoechst 33342,TUNEL(末端脱氧核苷转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术）等技术观察SCI后4h,8h,3d,7d,14d,21d及28d时损伤中心及邻近节段脊髓细胞的凋亡，治疗组损伤后30min给予大剂量MP，比较MP治疗组与损伤组脊髓细胞凋亡的变化，同时平行观察大鼠神经学和组织学恢复情况及两组神经丝蛋白（NF）含量的变化。结果：假损伤组各检测方法未见脊髓细胞凋亡，损伤组大鼠急性SCI后1d开始出现脊髓细胞凋亡，3d达高峰，自损伤中心向头尾端递减分布，持续21d,MP治疗组在伤后3d及7d凋亡脊髓细胞较损伤组显著减少，神经学恢复及组织学评分较损伤组有显著性提高，结论：凋亡是SCI后脊髓神经元死亡的一种重要方式，在继发性损伤中起极为重要的作用。MP的治疗作用可能与其干预SCI后细胞凋亡有关。

Neural cell apoptosis following acute traumatic spinal cord injury in rats and preventive effect of methylprednisolone

Objectives:To investigate the mechanisms of the sequential effects of neuron and glial cell apoptosis were observed after acute traumatic SCI in rats and the treatment effect of MP.Method:Impact injury of spinal cord was induced using the weight drop device modified by Allen technique.The neuronal and glial cell apoptosis in injuried spinal cord and adjacent tissue were examined by HE,Hoechst 33342,TUNEL and DNA ladder.High dose MP was administered at 30 min after SCI.The effects of MP on the apoptosis,neurological result,spared tissue of rim and the loss of neurofilament protein content of injuried cord were compared.Result:Apoptosis cells were noted primarily at 1d after injury,with a maximum presence in lesion center at 3d after injury,which spread to rostral and caudal areas and gradually disappear,lasted for 21d after injury.The apoptotic index of MP-treated group has distinctly less than that of SCI-group in 3d and 7d after injury,and MP group has a better result of neurological recovery and spared tissue.Conclusion:The temporal and spatial profiles of apoptotic cells in an experimental spinal cord injury provide a powerful evidence that apoptosis is an important death patterns of neurons and glias in injuried cord.Apoptosis play an important role in secondary progress after initial injury.Given the delayed time course of cell death,the apoptotic death of neurons and glial cells may be amenable to pharmacological intervention with subsequent improvement in functional recovery.One of the mechanisms of action of MP in SCI is due partially to the effect on preventing the apoptosis after SCI in rats.