Abstract
This study was performed to determine whether dexamethasone (DEX) had an effect on calcium-activated potassium channels (KCa channels) in blood-brain tumor barrier (BTB).Using a rat brain glioma model, we found that the expression of KCa channels protein was significantly increased in brain tumor tissue. And bradykinin-induced increase of KCa channels protein was further enhanced after DEX pretreatment for 3 days. In addition, DEX pretreatment enhanced bradykinin-mediated up-regulation of the density of IKCa 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-KCa channels.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents, Hormonal / pharmacology*
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Blood-Brain Barrier / drug effects*
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Blood-Brain Barrier / metabolism
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Bradykinin / pharmacology
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Brain / drug effects*
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Brain / metabolism
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Brain Neoplasms / drug therapy
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Brain Neoplasms / metabolism*
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Capillary Permeability
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Cell Line, Tumor
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Central Nervous System Agents / pharmacology
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Dexamethasone / pharmacology*
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Disease Models, Animal
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Female
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Glioma / drug therapy
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Glioma / metabolism*
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Membrane Potentials / drug effects
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Neoplasm Transplantation
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Potassium Channels, Calcium-Activated / metabolism*
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Random Allocation
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Rats
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Rats, Wistar
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Up-Regulation / drug effects
Substances
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Antineoplastic Agents, Hormonal
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Central Nervous System Agents
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Potassium Channels, Calcium-Activated
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Dexamethasone
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Bradykinin