尼莫地平对缺氧缺血性脑损伤后细胞凋亡基因的影响  

A study on the change of apoptotic genes and treatment effect of Ca^(2+)tagonist (Nimodipine) in hypoxic-ischemic brain damage of neonatal rats

作　　者：濮海平 刘华 侯琳[2] 于晓燕 

机构地区：[1]401医院儿科,山东青岛266071 [2]青岛大学医学院生化教研室,山东青岛266031

出　　处：《实用医药杂志》2007年第11期1352-1354,共3页Practical Journal of Medicine & Pharmacy

摘　　要：目的探讨新生鼠缺氧缺血性脑损伤(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 study the relationship between expression of Bcl-2,Bax and apoptosis of neonatal rats after hypoxic-lschemic brain damage（HIBD） and effects of Ca^2＋tagonist on them. Methods An animal model of neonatal hypoxic-isehemia blain damage was established. TUNEL （terminal- deoxynucleotldy transferase mediated nick end labeling）and immunohistochemical methods were used to detect apoptosis and Bcl-2,Bax in different time.Results A shift in ratio of Bcl-2 to 13ax might contribute to neuronal apoptosis after HIBD.Overexpression of Bel-2 protected cell from apoptosis,but Bax might be the function as a cell death effector protein.lnununostainiug of Bel-2 protein was increased while the Bax protein were decreased wilh the treatment of CaZ＋lagonist after HIBD.Ca^2＋tagonist decreased the apoptosls of cerebral cells.Conclusion Ca2qagonist may decrease the apoplosis by effect Bcl-2 and Bax.

关 键 词：CA^2+拮抗剂 缺血缺氧性脑损伤 BCL-2基因 凋亡 

分 类 号：R743[医药卫生—神经病学与精神病学] R-33[医药卫生—临床医学]