大鼠脊髓慢性压迫及减压后神经细胞凋亡及其相关基因的表达

目的：观察慢性压迫性脊髓损伤后及减压后神经细胞凋亡和Bcl-2mRNA，P53mRNA,CASPASE-3神经功能恢复的影响。方法：将55只同龄Wistar大鼠，置入后路渐进式压迫装置，制作成慢性压迫性脊髓损伤模型。随机分为假手术对照组（A组5只），慢性脊髓压迫组（B组25只），减压组（C组25只）。应用原原位末端脱氧核糖核苷酸转移酶介导dUTP标记（TUNEL）技术及原位杂交检测方法，观察各组细胞凋亡率及细胞凋亡相关基因Bcl-2mRNA、P53mRNA、CASPASE－3在慢性压迫性脊髓损伤后及减压后的表达，分别于损伤后及减压后1、3、7、14、28d对慢性脊髓损伤区进行细胞凋亡及原位杂交检测。结果：A、B、C三组均发现神经细胞凋亡及细胞凋亡相关基因Bcl-2mRNA、P53mRNA，CASPASE－3的表达，A、B、C三组细胞凋亡率及阳性细胞灰度值比较，差异有显著性意义（P＜0．05）。阳性细胞表达程度与细胞凋亡的减少及神经功能的恢复相一致。结论：慢性压迫性脊髓损伤可导致大量的神经细胞凋亡，同时激活内源性保护机制，使脊髓发生适应性改变，减压可能通过激活此机制而减轻神经细胞凋亡，起到保护作用。

Expression of apoptosis correlated gene after chronic compressive spinal cord injury and decompression

Objective:To explore the apoptosis and the effect of nervus functional recovery by Bcl-2mRNA,P53mRNA,CASPASE-3 after chronic compressive spinal cord injury and decompression.Method:55 Wistar rats were divided into 3 groups,control group (Group A) and chronic compressive spinal cord injury group (Group B) and decompression group (Group C).The cell apoptosis of spinal slice from the chronic compression injured spinal cord was examined by the terminal deoxynucleotidal transferase-mediated DUTP-biotin nick end labeling (TUNEL)reaction,and the neurological function was measured at 1,3,7,14 and 28 days post-operatively and 1,3,7,14 and 28 days post-decompression.BCL-2mRNA,P53mRNA,CASPASE-3 was examined by hybridization in situ.The positive cells were quantitated by a computer image analysis system.Result:Positive expression of apoptotic cell and BCL-2mRNA,P53mRNA,CASPASE-3 appeared both in Group A,Group B and Group C.There was significant statistic difference between Group A,Group B and Group C(P<0.05).The expression of positive cell was paralleled by the decrease of cell apoptosis and was paralleled by the significant improvement in neurological function evaluated by open-field and inclined plane tests.Conclusion:The chronic compression spinal cord injury can induce apoptosis and activate entogenous protective mechanisms in spinal cord.Decompression can inhabit apoptosis by activating this protective mechanism after CCSCI.