摘要
目的通过比较老年小鼠与青年小鼠海马区中细胞凋亡相关分子、神经再生相关分子的表达,探讨全脑缺血再灌注对老年鼠海马区神经再生与细胞凋亡的影响。方法 18月龄雄性ICR小鼠与2月龄雄性ICR小鼠各15只,随机分为假手术组、缺血再灌注3d组和缺血再灌注7d组,采用二血管加低血压法制作全脑缺血再灌注模型,Western blot检测海马组织中细胞凋亡相关分子BAX、Bcl2、caspase9,神经再生相关分子nestin、doublecortin的表达。结果全缺血再灌注后,老年鼠海马区细胞凋亡相关分子BAX、Bcl2、caspase9的表达均显著高于青年鼠,而神经再生相关分子nestin、doublecortin的表达均较青年组低。结论缺血再灌注损伤促进老年鼠海马区细胞凋亡,并影响海马区神经再生能力,削弱组织的自我修复和功能恢复。
Objective To investigate the effects of cerebral ischemia-reperfusion on apoptosis and neurogenesis in the hippocampus of aged mice,the expressions of molecules associated with apoptosis and neurogenesis were compared between aged mice and young mice.Methods 18-month-old and 2-month-old male ICR mice were randomly divided into sham group,I/P 3-day group and I/P 7-day group.The animal model of cerebral ischemia-reperfusion was established by means of two-vessel occlusion adding hypotension.Western blotting was employed to detect the expression of apoptosis or neurogenesis molecules,including Bax,Bcl2,caspase9,nestin and doublecortin.Results For cerebral ischemia-reperfusion injury,the expression of apoptosis-related molecules-Bax,Bcl2,caspase9-in the hippocampus of aged mice was higher than those of young mice.But the neurogenesis-related molecules,nestin and doublecortin,of aged mice were lower than those of young mice.Conclusion Ischemia-reperfusion injury increases apoptosis and decreases the neurogenesis ability of aged mice in the hippocampus,which weakens the self-healing ability of injured tissue.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2014年第6期501-505,共5页
Chinese Journal of Histochemistry and Cytochemistry