大鼠脑创伤细胞凋亡和bcl-2基因家族表达的变化  

Apoptosis of brain cells and expression changes of bcl-2 gene family after traumatic brain injury in rats

作　　者：杨云华[1] 张可成[2] 张艺梅[3] 

机构地区：[1]成都军区昆明总医院神经外科,云南昆明650032 [2]第三军医大学新桥医院神经外科,重庆400037 [3]解放军第60医院外科,云南大理671003

出　　处：《西南国防医药》2009年第5期488-491,共4页Medical Journal of National Defending Forces in Southwest China

摘　　要：目的:研究创伤性脑损伤(TBI)脑细胞凋亡发生及bcl-2基因家族表达变化,揭示TBI后继发性脑损伤的发生机制。方法:建立大鼠TBI模型,运用组织原位标记凋亡细胞检测、免疫组织化学等技术,观察TBI后1～14d大脑伤侧皮层和海马等脑区细胞凋亡及bcl-2、bax基因表达的变化。结果:TBI后伤侧大脑广泛存在凋亡现象,以皮层及海马为甚;伤后1d即出现凋亡细胞,3d达高峰,7～14d逐渐恢复正常;TBI后bcl-2、bax基因在伤脑表达增高,其增高的时相与凋亡规律相似,表达与细胞凋亡发生呈正相关。结论:细胞凋亡参与TBI后脑细胞的死亡机制,bcl-2基因在TBI后的脑组织中表达增加,对细胞凋亡发生有抑制作用;bax可促进细胞凋亡,TBI后表达明显增加,参与TBI后细胞凋亡的正向调节,可能是脑创伤后细胞死亡的重要机制。Objective： To investigate the apoptosis of brain cells and expression changes of bcl - 2 gene family after traumatic brain injury（TBI） in rats, and to study the mechanism of secondary brain injury after TBI. Methods：After TBI model of rats were established, the apoptosis of brain cells and expression levels of bcl - 2 and bax gene in injured brain side（ cortex, hippocampus area, etc）in 1 - 14 days were evaluated by TdT - mediated dUTP nick end labeling （TUNEL） and immunohistochemistry （ IHC ）, respectively. The relationship between TUNEL and IHC staining results was also analyzed. Results ： TUNEL staining results showed that apoptotic cells were widespread in brain after TBI, and there were more apoptotic calls in injured cortex（IC） and hippocampus CA area（CA） than those in normal areas. The number of apoptotic cells increased on the first day after TBI, reached peak on the third day, and then declined gradually in seven to fourteen day after TBI. IHC staining results demonstrated that the expression levels of bcl - 2 and bax gene increased significantly in brain after TBI. Moreover,their increasing and decreasing time points were similar to those of apoptotic cells. The expression levels of bcl - 2 and bax gene were positively correlated with the number of apoptotic cells. Conclusion： Apoptosis may contribute to the brain cells death, and beth the bcl - 2 and bax expression, appears to increase after TBI. The bcl - 2 expression can inhibit the apoptosis, but the bax expression can promote the apoptosis through up - regulation of the apoptosis after TBI and it may be an important factor for cells death after brain trauma.

关 键 词：创伤性脑损伤 凋亡 BCL-2基因 BAX基因 大鼠 

分 类 号：R651.1[医药卫生—外科学]