甲基强的松龙对急性脊髓损伤神经元保护作用的实验研究

The experimental study of methylprednisolone on protecting neurons after spinal cord injury in rats

目的探讨甲基强的松龙对急性脊髓损伤(ASCI)后神经元是否具有保护作用。方法大鼠随机分为2组,即模型组和正常对照组(N组),模型组建立脊髓半横断损伤模型后又分两组,即激素治疗组(M组),腹腔注射甲基强的松龙(MP);模型对照组(B组)术后不做处理。每组大鼠观察损伤后3d、7d、15d和30d。取脊髓损伤部位标本做光镜病理组织学检查,观察正常神经元和变性神经元的数量变化。结果⑴B组在ASCI早期脊髓损伤区的灰白质被明显的破坏,有出血及坏死,可见多量空泡状细胞和溃变的神经纤维,部分组织液化。在损伤灶内见正常神经元及神经纤维的数量稀少,多数神经元呈现不同程度的变性乃至坏死。随着时间的延长,神经元数量进一步减少,胶质细胞增生形成疤痕,或者液化形成囊腔。病变常常累及对侧组织,而M组的脊髓损伤区组织结构的变化与B组基本相同。⑵在ASCI后3d,M组的正常神经元数量少于B组,变性神经元数量与B组相近;在损伤7d以后,随着时间的延长,B组的变性神经元数量减少的同时,正常神经元的数量稍有减少,而M组的变性神经元数量减少的同时,正常神经元数量有所增加。结论⑴MP对ASCI后的继发性组织结构破坏无明显的改善作用;⑵MP在ASCI早期能促使神经元的死亡,但在后期能增加正常神经元的数量,其机理有待于进一步研究。

Objective To study the effect of Methylprednisolone on protecting the neuron after spinal cord injury in rats. Methods Rats were randomly divided into two groups, including normal group(N) and model group. The latter group were hemitransected at the T12 level and then also randomly divided into 2 groups: methylprednisolone(MP)group were injected MP in peritoneal cavity(M) and model control group (B) were not treatel. The histopathological changes of the injured site of spinal cord in each group were observed by optical microscope with 3 day, 7 day, 15 day and 30 day after injury, and the number of normal and degenerative neurons were analysed. Results ⑴ The construct in the area of injured spinal cord could be obviously destroyed and many pathological changes seen at the early period of postinjury such as haemorrhage , necrosis ,liquefaction, empty cell soakage and degeneration of nerve fiber . Normal neuron and nerve fiber could not be seen in area of injured tissue and barely seen near the injured area. The majority of neurons became denatured and even death. With the time going, reactive astrogliosis became compact scar. The area of the spinal cord injured was similar in B and M group and almost involved the left side of cord; ⑵ At 3 day of postinjury the number of normal neuron in M group was less than that in B group and degenerating neuron was near to B group, but the late with the degenerating neuron became less the number of normal neuron increased in M group and decreaced in B group.Conclusions ⑴ MP can not improve the secondary spinal cord injury afterASCI; ⑵ MP had no protective ability for neuron at the early period of ASCI and even accelerate death of neuron, but it can increase the number of normal neurons at the late stage of ASCI and the mechanism needs further study.