摘要
目的 探讨地塞米松（ＤＥＸ） 预处理神经保护作用的可能机制。方法 在建立新生大鼠脑缺氧缺血（ＨＩ） 损伤标准动物模型（７ｄ 龄新生大鼠，结扎其一侧颈总动脉后予缺氧２．５ｈ）基础上，运用ＨＥ染色光镜观察及原位末端标记技术，观察分析缺氧缺血组、预给药组（ＤＥＸ预处理后予缺氧缺血） 、后给药组（ 缺氧结束后即刻予ＤＥＸ） 、假手术给药组（ 仅作颈正中切口后即缝合皮肤，不结扎颈动脉，假手术前１２ｈ 予注射ＤＥＸ） 以及正常对照组共５ 组新生大鼠的缺氧缺血侧大脑组织细胞凋亡情况。结果 在ＨＩ前给予ＤＥＸ 预处理能显著减少脑细胞的凋亡，而ＨＩ后给予ＤＥＸ 则对细胞凋亡无明显影响。结论 ＤＥＸ 预处理对神经的保护作用可能是通过抑制细胞凋亡而实现的。
Objective To investigate the possible mechanisms of the neuroprotective effect of dexamethasone (DEX) on neonatal rats following cerebral hypoxia ischemia. Methods The apoptosis at ipsilateral cerebral hemisphere was analyzed by hematoxylin eosin staining and ISEL in these five groups of neonatal rats with hypoxia ischemia, pretreatment with DEX prior to hypoxia ischemia, treatment with DEX immediately following HI, pretreatment with DEX prior to sham and normal controls, respectively. Results Pretreatment with DEX could markedly reduce brain cells apoptosis while treatment with DEX immediately following HI had no effect in the study. Conclusion The neuroprotective effect of DEX given before HI may be induced through inhibition of apoptosis.(Shanghai Med J, 2000, 23∶81 83)
出处
《上海医学》
CAS
CSCD
北大核心
2000年第2期81-83,共3页
Shanghai Medical Journal
关键词
脑缺氧
脑缺血
神经元死亡
地塞米松
Cerebral hypoxia
Cerebral ischemia
Apoptosis
Delayed neuron death
In situ end labelling
