The regulatory effects of dexamethasone on the expression of bcl 2 mRNA in neonatal rats following cerebral hypoxia ischemia

Objective To investigate the possible mechanism of the neuroprotective effect of dexamethasone (DEX) on neonatal rats following cerebral hypoxia ischemia. Methods Rapid competitive reverse transcriptase PCR was used to analyse the expression of bcl 2 mRNA at ipsilateral cerebral hemisphere semi quantitatively in neonatal rat models of hypoxia ischemia, pre treatment with DEX prior to hypoxia ischemia; treatment with DEX immediately following hypoxia ischemia; pre treatment with DEX prior to sham and normal controls, respectively. Results The expression of bcl 2 mRNA in the ipsilateral hemisphere following cerebral hypoxia ischemia, began at 6h after recovery, peaked at 12h, decreased to lower level at 24h, and returned towards baseline at 72h (n=3/time point). The expression of bcl 2 mRNA in the ipsilateral hemisphere induced by hypoxia ischemia could be inhibited by pretreatment with DEX prior to hypoxia ischemia at the early stage of recovery, but the induction of bcl 2 mRNA began at 24h, and lasted at least 7 days after recovery. DEX administered to the rats immediately following hypoxia ischemia had no effect on the expression of bcl 2 mRNA. Conclusion Pretreatment with DEX exerts neuroprotective effect on neonatal rats following hypoxia ischemia, partially through positive induction of the expression of bcl 2 mRNA.