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目的探讨地塞米松（ＤＥＸ）预处理对缺氧缺血新生大鼠脑保护作用的可能机制。方法建立新生大鼠缺氧缺血性脑病动物模型，应用快速竞争性逆转录聚合酶链反应（ＲＴＰＣＲ）技术，分别对缺氧缺血、ＤＥＸ预处理后予缺氧缺血、缺氧结束后即刻予ＤＥＸ、ＤＥＸ加假手术、正常对照５组动物的实验侧大脑组织中ｂｃｌ２ｍＲＮＡ的表达进行半定量分析。结果缺氧缺血后，新生大鼠脑ｂｃｌ２ｍＲＮＡ的表达自再灌注后６小时开始明显增强，１２小时达高峰，２４小时回落至较低水平，至７２小时已基本检测不到。而ＤＥＸ预处理在再灌注早期可抑制缺氧缺血对脑ｂｃｌ２ｍＲＮＡ表达的诱导，但自再灌注后２４小时始刺激ｂｃｌ２ｍＲＮＡ的表达，并持续至再灌注７天以后。缺氧结束后即刻给予ＤＥＸ对ｂｃｌ２ｍＲＮＡ的表达无影响。结论ＤＥＸ预处理对脑缺氧缺血新生大鼠的神经保护可能部分是通过对抗凋亡基因ｂｃｌ２的正向调节而实现的。
Objective To investigate the possible mechanism of dexamethasone (DEX) preconditioning on cerebral protection in neonatal rats with hypoxic-ischemic brain damage. Methods Animal models of hypoxic-ischemic encephalopathy were established in neonatal rats. The rapid reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the effects of hypoxia-ischemia, DEX pretreatment on hypoxia-ischemia, Immediately after the end of oxygen to DEX, DEX plus sham operation, the normal control group 5 experimental animal side of the brain tissue bcl 2 mRNA expression semi-quantitative analysis. Results After hypoxia-ischemia, the expression of bcl-2 mRNA in neonatal rat brain increased significantly from 6 hours after reperfusion, reached the peak at 12 hours, dropped to a lower level at 24 hours, and basically undetectable to 72 hours. However, DEX pretreatment inhibited the expression of bcl 2 mRNA in the early stage of reperfusion, but stimulated the expression of bcl 2 mRNA 24 hours after reperfusion, and continued until 7 days after reperfusion. Immediately after hypoxia given DEX bcl 2 mRNA expression was not affected. Conclusion Neuroprotection of DEX preconditioning on neonatal rats with hypoxic-ischemic brain damage may be partially achieved through the positive regulation of the anti-apoptotic gene bcl-2.