These data suggested that following hypoxia / reoxygenation , over - activity of bkca channels may mediate cultured hippocampal neuronal apoptosis induced by hypoxia / reoxygenation via activation of caspase - 3 X现diazoxide或valinomycin均可诱导正常培养的神经元凋亡及激活caspase上。上述结果表明缺氧复氧可能引起bkc 。
2.
Furthermore , k + ionophore valinomycin and k + channel opener diazoxide alone induced neuronal apoptosis and caspase - 3 activation . besides , katp channel blockers tolbutamide and glybenclamide also showed neuroprotective effects and decreased caspase - 3 activation after hypoxia / reoxygenation . while the role of katp channels in neuronal apoptosis is not clear 为进一步证实钾通道在缺氧复氧诱导的神经元凋亡中的作用，我们采用了钾通道开通剂100pmdiazoxide及钾离子载体50nmvallnomycln 。
