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Severe hypoxia can induce the blood-brain barrier (BBB) disruption and cerebral edema, even cerebral hernia and death.Hypoxia-inducible factor-1α (HIF-1α) is one of the most important factors for the cellular response to hypoxia.Inhibition ofHIF-1αean amelioratethe BBB dysfunction and reduce the permeability of vascular endothelial cells in hypoxia.Recent researches showed that Minocycline was not only a kind of antibiotics, but also able to promote HIF-1α degradation and inhibit angiogenesis when a lack of oxygen.Forsurveying theeffect of Minocycline to highvascular permeability and HIF-1α induced by hypoxia.UsingTrans Epithelial Electric Resistance(TEER), Evans blue and Transmission electron microscopy (TEM), we firstlyfound that Minocycline decreasedthe vascular permeability of brain induced by hypoxia in vitro (1% O2) and in vivo (8000 m).Meanwhile, we discovered that Minocycline regulated HIF-1α in protein level rather than in genetic level, while Minocyclinedecreased the expression of matrix metallproteinases (MMP-2 and MMP-9) and up-regulated tight junction proteins (TJS) both in protein and genetic level.