The regulatory effects of dexamethasone on mRNA expression of bcl-x and bax in neonatal rats with cerebral hypoxia-ischemia

Objective To explore the possible mechanisms of the neuroprotective effect of dexamethasone (DEX) on neonatal rats with cerebral hypoxia-ischemia. Methods The rapid competitive reverse transcriptase-PCR was used to analyze the expression of bcl-x (bcl-xl and bcl-xs) and bax mRNA at ipsilateral cerebral hemisphere semi-quantitatively in the neonatal rat model of hypoxia-ischemia ( HI group) , DEX treatment prior to hypoxia-ischemia (DH group) , DEX treatment immediately following hypoxia-ischemia (HD group) , DEX treatment prior to sham operation and normal controls, respectively. Results The expressions of bcl-x and bax mRNA in the ipsilateral hemisphere following cerebral hypoxia-ischemia increased significantly, and reached the peak level at 24h (bcl-x was 1.52 ± 0.17 and bax was 1.43 ± 0.17) . During 2 h to 72 h following hypoxia-ischemia, the expressions of bcl-x and bax mRNA in DH group (bcl-xs were significantly lower than those in HI group (bcl-xs: 0.03±0.05 ~0.19±0.23 vereus 0.14±0.06 ~ 1.52 ± 0.17, and bax: 0.02 ± 0.03 ~ 0.13 ± 0.21 versus 0.09 ± 0.03 ~1.43 ± 0.17, respectively, P 0.05) . DEX and HI had no evident effect on the expression of bcl-x mRNA. Conclusion Cerebral HI could induce the overexpressions of bax and bcl-x mRNA, which could play an important role in the regulation of apoptosis following cerebral HI. Pretreatment with DEX could exert the anti-apoptotic role by the down-regulation of bax and bcl-xs gene expressions. Key words: Cerebral anoxia; Cerebral ischemia; Dexamethasone; Bcl-x; Bax