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机构地区:[1]浙江大学医学院附属第二医院神经外科,杭州310009
出 处:《中华急诊医学杂志》2004年第2期100-102,共3页Chinese Journal of Emergency Medicine
基 金:浙江省医学科研基金 ( 2 0 0 0A110 )
摘 要:目的 探讨严重颅脑损伤后Bcl 2、Bax基因表达与细胞凋亡的关系。方法 采用改进的Feeney自由落体损伤模型 ,应用分子生物学方法———脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(terminal deoxynucleotidyltransferasemediatednickendlabeling,TUNEL)以及免疫组织化学方法 ,对 5 0只严重颅脑大鼠脑组织中的凋亡细胞和Bcl 2、Bax免疫反应阳性的细胞进行观察、统计。结果 损伤组大鼠脑组织中凋亡细胞数明显高于未损伤组 ,Bcl 2、Bax表达也有所增加 ,同时 ,损伤组Bax/Bcl 2阳性细胞数的比值明显大于未损伤组。结论 BclObjective To discuss the relationship between expression of Bcl-2,Bax and apoptosis after severe brain injury. Methods 50 rats were experimented, which were injured in the brain. TUNEL (terminal-deoxynucleotidyl transferase mediated nick end labeling) and immunohistochemisty were used to detect apoptosis and Bcl-2, Bax expression in all the brain tissue.Results There were significant differences between the injury group and noninjury group with more TUNEL?Bcl-2 Bax positive cells in the injured rats. And in injured rats the value of Bax/Bcl-2 was larger than that in uninjured rats.Conclusion Disequilibrium between the Bcl-2 and Bax may be the reason of promoting apoptosis after severe brain injury.
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