大鼠脑损伤后脑神经细胞内bcl-2和bcl-xL水平的变化及意义

Expression and significance of bcl-2 and bcl-xL in rat neuron after acute brain trauma

目的 观察大鼠急性脑损伤后脑神经细胞内bcl 2、bcl xL的表达状况及意义。 方法55只大鼠采用弥漫性脑损伤模型制成轻、重度 2组大鼠脑损伤模型 ,以免疫组化方法 ,检测脑神经细胞中bcl 2、bcl xL的表达水平 ;以原位细胞凋亡 (TUNEL)法检测神经细胞凋亡水平。 结果 正常大鼠神经细胞中很少有bcl 2表达 (额顶区 4 40± 1 67,海马区 3 2 0± 1 30 ) ;但可见bcl xL表达 (额顶区45 60± 4 34 ,海马区 50 2 0± 3 50 )。大鼠大脑遭受打击后 ,神经细胞bcl 2表达明显增高 ,以伤后第 1天最为明显 (轻度组 :皮层 :30 0± 4 3 ,海马 :46 6± 3 2 ) ,轻度组高于重度组。各观测时间点bcl 2表达水平与神经细胞凋亡水平呈负相关 (r在 - 0 847～ - 1 0 0 0之间 ,P <0 0 1 ,n =1 0 )。bcl xL表达变化不明显。 结论 大鼠急性脑损伤后脑神经细胞内bcl 2表达增高 ,而bcl xL在损伤后变化不大 。

Objective To observe the expression of bcl 2 and bcl xL in rat brain neuron after acute brain trauma Methods The rat model of mild and sever brain trauma were made by diffused brain injury. The expression of bcl 2 and bcl xL in rat brain neuron was examined by immunohistriochemical staining. Rat neuron apoptosis was detected by TUNEL method Results There were few bcl 2 (cortex: 4 40±1 67, hippocampal: 3 20±1 30) and lots of bcl xL (cortex: 45 60±4 34, hippocampal: 50 20±3 50) expression in normal controls. After impact, the expression of bcl 2 in rat brain neuron increased, most distinctly on day 1(cortex: 30 0±4 3, hippocampal: 46 6±3 2), in mild group A negative correlation was seen between bcl 2 expression and neuronal apoptosis (-1< r <-0 847, P <0 01, n =10). No change was seen in bcl xL expression Conclusions bcl 2 expression increased after acute brain trauma but bcl xL did not change much. Both bcl 2 and bcl xL are concerned with anti apoptosis in neuron after acute brain trauma