Abstract
This study was performed to determine whether dexamethasone (DEX) had an effect on calcium-activated potassium channels ( K Ca channels) in blood-brain tumor barrier (BTB). Using a rat brain glioma model, we found that the expression of K Ca channels protein was significantly increased in brain tumor tissue. And bradykinin-induced increase of K Ca channels protein was further enhanced after DEX pretreatment for 3 days. In addition, DEX pretreatment enhanced bradykinin-mediated up-regulation of the density of I KCa in the rat brain C6 cells in vitro BTB. Bradykinin markedly increased BTB permeability independent of DEX pretreatment. All of these results strongly suggest that DEX could regulate the target in the transcellular pathway of BTB- K Ca channels.
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