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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 mechanism of neuroprotective effect of dexamethasone (DEX) preconditioning. Methods Based on the establishment of a standard animal model of hypoxic-ischemic brain damage (HI) in neonatal rats (7d-old neonatal rats with hypoxia 2.5h after ligation of one common carotid artery), HE staining and light microscopy In situ end labeling technique was used to observe and analyze the effects of hypoxic-ischemic preconditioning, hypoxic-ischemic preconditioning and DEX preconditioning, post-hypoxia-ischemia (DEX) and sham operation Only for the neck incision after suture the skin, without carotid artery, 12h before sham surgery to inject DEX) and normal control group of 5 neonatal rats hypoxic ischemic brain tissue apoptosis. Results Pretreatment with DEX could significantly reduce the apoptosis of brain cells, while the dexamethasone treatment with DEX had no significant effect on apoptosis. Conclusion The protective effect of DEX preconditioning on the nerve may be through the inhibition of apoptosis.