新生鼠缺血再灌注脑损伤后细胞凋亡相关基因表达及Ca^(2+)拮抗剂的作用  

Change of apoptotic genes and treatment effect of GM1 on hypoxic ischemic brain damage of neonatal rats

作　　者：刘华[1] 濮海平[1] 于晓燕[1] 郭萍[1] 

机构地区：[1]青岛市解放军第401医院儿科,山东青岛266071

出　　处：《中国儿童保健杂志》2007年第5期505-506,509,共3页Chinese Journal of Child Health Care

摘　　要：【目的】探讨新生大鼠缺氧缺血性脑损伤(hypoxic-ischemia brain damage,HIBD)后Bcl-2、Bax基因表达与细胞凋亡的关系及Ca2+拮抗剂对其的影响。【方法】建立新生鼠HIBD动物模型,用TUNEL法和免疫组化法观察缺氧缺血和Ca2+拮抗剂干预后不同时间点细胞凋亡情况及凋亡基因Bcl-2、Bax的变化。【结果】缺氧缺血组随时间延长脑组织中Bcl-2、Bax的表达增加,Bcl-2/Bax的比值下降,同时凋亡细胞数增加,表明Bcl-2、Bax两者比值的降低促进凋亡的发生。Ca2+拮抗剂干预组Bcl-2表达增加显著,降低了Bax的表达,凋亡细胞减少。【结论】Ca2+拮抗剂可能通过改变凋亡基因的表达而抑制神经细胞的凋亡过程。[Objective] To discuss the relationship between expression of Bcl-2,Bax and apoptosis of neonatal rats after cerebral hypoxic-ischemia（HI） and effects of Ca^2＋ tagonist on them. [Methods] An animal model of neonatal hypoxic-ischemia biain damage（HIBD） was established. TUNEL（terminal-deoxynucleotidy transferase mediated nick end labeling）and immunohistochemical were used to detecte apoptosis and Bcl-2,Bax in different time. [Results] A shift in ratio of Bcl-2 to Bax might contribute to neuronal apoptosis after HI. Overexpression Of Bcl-2 protected cell from apoptosis but Bax might be function as a cell death effector protein. The study showed that immunostaining of Bcl-2 protein was increased while the Bax protein were decreased with the treatment of Ca^2＋ tagonist after HI. Ca^2＋ tagonist decreased the apoptosis of cerebral cells. [Conclusion] Ca^2＋ tagonist may decreas the apoptosis by effect Bcl-2 and Bax.

关 键 词：CA^2+拮抗剂 脑缺氧 脑缺血 BCL-2基因 凋亡 

分 类 号：R722.1[医药卫生—儿科]