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 24 h (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 versus 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, P0.01). While there were no significant differences in the expressions of bcl xs and bax mRNA between HD group (0.13±0.07～1.53±0.18 and 0.07±0.05～1.47±0.10, respectively) and HI group (P0.05). 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.