Research On Sevoflurane Preconditioning To Anti-apoptosis Of Hippocampal Neurons By Hypoxia-reoxygenation In Rats

Objective To observe the effect of sevoflurane and 5-HD preconditioning to anti-apoptosis of hippocampal neurons by hypoxia-reoxygenation in rats, and to investigate the optimal concentration of sevofluance in neuroprotective effect and its possible molecular mechanism. Method Isolated cultured hippocampal neurons of SD rat which were borned in 24h, female and male not confined, body weight from 5-6 gramme, were assigned into the following seven groups randomly: Control group (Group A), Hypoxia-reoxygenation(HR) group (Group B), HR and sevoflurane 6% group (Group C), HR and sevoflurane 4% group (Group D), HR and sevoflurane 2% group (Group E), HR and 5-HD 100μmol/L group (Group F), HR and 5-HD 100μmol/L and sevoflurane 6% group (Group G), The hippocampal neurons were treated with diazoxide 30 min everyday for successive 3 days before being subjected to 4 h oxygen deprivation followed by 24 h reoxygenation. The neuronal vitality was assayed and apoptosis rate determined after 24 h reoxygenation. The expression of Akt, Bcl-2 and Bax protein was determined by western blotting. Results The vitality of hippocampal neurons in Group B was significant lower than that in Group A, whereas the apoptotic rate was opposite (P<0.01);The vitality of hippocampal neurons and the expression of Bcl-2,Akt protein in Group D were significant higher than that in Group E,whereas the apoptotic rate and the expression of Bax protein were opposite (P<0.01); the vitality of hippocampal neurons and the expression of Akt, Bcl-2 protein in Group D were significant lower than that in Group C, whereas the expression of Bax protein and the apopototic rat were opposite (P＜0.01); compare to group C,the vitality of hippocampal neurons and expression of Bcl-2, Ake protein in group G were significant weak while the apoptotic rat and the expression of Bax protein were significant higher. Conclusions Sevoflurane 6% inhaled preconditioning can obviously inhibit apoptosis of hippocampal neurons by hypoxia- reoxygenation in rats. The results also demonstrate that volatile anesthetic-induced neuroprotective preconditioning is dose-dependent.The underlying mechanism may be related to activation of mitoK∧Tp signal transduction passageway, the up-regulation of Bcl-2 protein expression and the down-regulation of Bax protein expression.