[Bax is involved in K ATP-mediated protection of the hippocampal neurons against hypoxic exposure].

To investigate the mechanism of K(ATP)-mediated protection of the hippocampal neurons exposed to hypoxia.,The neurons were exposed to hypoxia (0% O(2), 5% CO(2) and 95% N(2)) or treated with tolbutamide or diazoxide for 12 or 24 h 1 week after seeding. MTT assay was used to measure the cell viability. RT-PCR was performed to detect Bax mRNA expression.,MTT assay showed a much lower survival rate (75.7-/+2.8%) of the neurons exposed to severe hypoxia (PO(2)=0 mmHg) than that of the neurons in normoxia (P<0.01, n=7). Tolbutamide (100 micromol/L) treatment significantly reduced the survival rate of the neurons to (55.7-/+2.5)%, while diazoxide (100 micromol/L) increased the survival rate to 81.1-/+2.4)% (P<0.01, n=6). In normoxia, neither diazoxide nor tolbutamide significantly affected the cell viability (P>0.05, n=6). A significant increase in Bax (P<0.01) and Fas (P<0.01) mRNA expression occurred in the neurons exposed to severe hypoxia (PO(2)=0 mmHg) as compared with the expressions in cells in normoxia (PO(2)=144 mmHg). In the hypoxic neurons, tolbutamide significantly increased Bax mRNA expression(P<0.05), while diazoxide reduced the expression to a level comparable with that observed in normoxic condition. CONCLUSION Bax is involved in KATP-mediated protection of hippocampal neurons exposed to hypoxia.