老龄大鼠脑缺血再灌注神经细胞凋亡、Bcl-2、Bax表达与caspase-3活性变化  

Age-related changes of expression of Bcl-2, Bax and caspase-3 activity after cerebral ischemia/reperfusion in aged rats

作　　者：李建生[1] 任小巧[1] 刘轲[1] 刘正国[1] 赵跃武[1] 孔令飞[1] 

机构地区：[1]河南中医学院老年医学研究所,河南郑州450008

出　　处：《中国病理生理杂志》2005年第10期2009-2013,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金(No.30371812);河南省高校创新人才基金(No.2000-10);河南省杰出青年基金(No.0412000800)资助

摘　　要：目的:研究老年与青年急性局灶性脑缺血及再灌注(L／R)后细胞凋亡、Bcl-2、Bax表达与caspase-3 活性变化的异同。方法:采用线栓法建立急性局灶性脑L／R模型,检测青年与老龄大鼠脑缺血3 h及L／R 3 h、6 h、12 h、24 h、72 h后脑梗死面积、神经细胞凋亡、Bcl-2、Bax表达及caspase-3活性。结果:老龄大鼠脑缺血3 h和L／R 12 h脑梗死面积较青年大鼠增大。随着I／R时间延长,细胞凋亡明显增加,老龄大鼠出现的早、持续时间长。青年大鼠 随着I／R时间的延长Bcl-2表达明显增强,老龄大鼠不明显。老龄大鼠L／R Bax表达早于青年大鼠,其表达增强及 持续时间较长。老龄大鼠L／R caspase-3的激活早于青年大鼠。结论:老龄大鼠L／R脑组织损伤严重,神经细胞凋 亡显著,其机制与Bax表达增加、casspase-3活性增高及其持续时间长有关。AIM： To study age - related changes of expression of Bcl - 2, Baxandcaspase-3 activity after focal cerebral ischemia/reperfusion （I/R） in aged rats, METHODS： The aged SD rats （20 - 21 months） and the young animals （4 - 5 months ） were subjected to 3 h of middle cerebral artery oceulsion with the intraluminal filament technique, followed by 3 h, 6 h, 12 h, 24 h and 72 h of refeffusion. Expression of Bcl - 2, Bax and caspase - 3 activity of the young and the aged rats were examined.RESULTS： Cerebral infarct zone increased in the aged at ischemia 3 h and I/R 12 h than that in the young. With I/R time longer, increase in neuron apoptosis showed early and lasted longer in the aged. The Bcl - 2 expression increased in the young with I/R time longer, but was not obvious in the aged. Bax expressd obviously and early, and kept on longer in the aged during I/R than that in the young. The enhanced activity of easpase - 3 showed early in the aged than that in the young during I/R. CONCLUSION： The mechanisms of serious cerebral injury and neuron apoptosis might be related to the increase in Bax expression and easpase - 3 activity.

关 键 词：脑缺血 再灌注 神经元 细胞凋亡 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]