环扎法致大鼠脊髓损伤早期减压后caspase-3的表达及其与神经细胞凋亡相关性研究

目的]探讨大鼠急性脊髓损伤后早期不同减压时间对神经细胞凋亡及caspase -3表达的影响.方法]采用环扎法大鼠急性脊髓损伤压迫模型.84只SD大鼠,随机分成4组,对照组即A组:行椎板减压；实验组分为B组:环扎术后8h行减压术；C组:环扎术后72 h行减压术；D组:环扎术后不行减压术.分别于手术后1、3、7、21 d行HE染色、免疫组化染色测定caspase -3的表达、原位末端脱氧核糖核酸转移酶介导的脱氧尿苷三磷酸(dUTP)标记法(TUNEL法)检测神经细胞的凋亡水平、行为学(BBB评分,斜板评分)观察大鼠神经功能恢复情况.结果]各组不同时间点BBB评分、斜板评分之间比较具有显著性差异(P＜0.05)；实验组caspase -3、Tunel阳性细胞均在术后1d增多、3d达高峰、7d表达减弱、21 d仍有表达；不同时间点caspase -3、Tunel阳性细胞数比较均具有统计学差异,二者成正相关(r =0.69 ～0.98,P＜0.05).结论]环扎法致大鼠脊髓损伤动物模型是一种理想的脊髓损伤造模方法.大鼠脊髓损伤早期减压可能阻止或减轻脊髓神经细胞凋亡.

Study of correlation between neural cell apoptosis and caspase-3 expression after rat cerclage-induced spinal cord injury model by different timing of early decompression

Objective] To study the apoptosis of neural cells and the changes of caspase-3 expression on early operative decompression after acute spinal cord injury(ASCI)in rats. Method]The model of spinal cord injury were established by cerclage-induced.Eighty-four SD rats were prospectively randomized to the control group(A) and experimental groups(B、C、D),namely,group A were laminectomy only.Groups B,C were decompressed for 8 hours、72 hours after cerclage-induced.Group D had no decompression.After surgery,BBB score,inclined plane score were observed with recovery of nerve function.HE and the expression of caspase-3 was detected by immunohistochemistry study at 1,3,7,21 days,the level of the neuronal cell was deleted by the terminal deoxynucleotidyl transferase-mediated DUTP nick end labeling(TUNEL)methods.Result] BBB score and inclined plane score were statistically different compared in each group(P<0.05).Experimental group,caspase-3,tunel positive cells were increased in 1 day,peaked in 3 days,decreased in 7 days and visibled in 21 days.At different time points in experimental group,caspase-3,tunel positive cells were statistically different,both positively correlated(r= 0.69-0.98,P<0.05). Conclusion]Spinal cord injury of cerclage-induced animal model in rats is an ideal way of modeling.Early decompression of spinal cord injury may prevent or reduce apoptosis of spinal cord nerve cells.