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脑缺血再灌注损伤的海马神经元对Bax、Bcl-2和Caspase-3的表达 被引量:7

Expression of Bax, Bcl-2 and Caspase-3 in hippocampal CA1 region following cerebral ischemia-reperfusion injury
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摘要 目的:凋亡调控基因在脑缺血再灌后海马神经元的表达。方法:采用免疫组织化学的方法,观察昆明小鼠双侧颈总动脉结扎7 min后不同再灌时间组(24 h组、48 h组、72 h组、7 d组、14 d组)海马CA1区神经元Bax、Bcl-2和Caspase-3的活性形式CM1的免疫反应活性。结果:Bax和CM1阳性神经元数在48 h组最多,与其他各组相比差异有显著性(P<0.01),72 h组明显下降,14 d组完全消失;而Bcl-2阳性神经元数在48 h组增多(与24 h组相比,P<0.01),72 h组下降,7 d组再次上升(与72 h组相比,P<0.01),14 d组最多(与48 h组相比,P<0.01)。在24 h、48 h、72 h、7 d组,Bax阳性神经元多于Bcl-2阳性神经元(P<0.05),14 d组则相反。结论:Bax和Caspase-3在脑缺血再灌早期表达增强,然后下降以至消失,Bcl-2于再灌后期表达增强。Bax表达上调可能与Caspase-3激活相关。 Objective:To explore the expression of apoptosis regulated genes of hippocampus after cerebral ischemia-reper-fusion. Methods: With immunohistochemical method, the immunoreponsive activity of Bax,Bcl-2 and CM1 (active form of Caspase-3) were observed in hippocampal CA1 region of Kunming mice following transient bilateral common carotid arteries (BCCA) ligation with 7 min and different reperfusion period (24 h,48 h,72 h,7 d, 14 d group). Results:The number of Bax and CM1 positive neurons was more in 48 h than all other ones (P< 0.01). Their expession decreased significantly in 72 h group,and could not be detected in 14 d group. The number of Bcl-2 positive neurons was increased in 48 h group (compared with the 24 h group,P<0.01) .which was decreased in 72 h group. However.it increased again in 7 d group, and reached the peak on 14 d. The number of Bax positive neurons was significantly more than the number of Bcl-2 positive neurons in 24 h,48 h,72 h,7 d,14 d group (P<0.05). On contrast,it was reverse in 14 d group. Conclusion:The expression of Bax and Caspase-3 is increased in early reperfusion period,so does the expression of Bcl-2 in late reperfusion period; and the expression of Bax exceeding Bcl-2 may be associated with the activation of Caspase-3.
出处 《解剖学杂志》 CAS CSCD 北大核心 2003年第1期21-25,共5页 Chinese Journal of Anatomy
基金 湖南省自然科学基金资助项目(编号:00JJY2069)
关键词 脑缺血 再灌注损伤 凋亡调控基因 BAX BCL-2 CASPASE-3 免疫组织化学 cerebrum hippocampus cerebral ischemia apoptosis Caspase-3 Kunming mouse
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