Objective      To determine the effect of sodium butyrate (NaB) on the permeability of vascular endothelial cells induced by hypoxia and investigate its underlying mechanism.       Methods      Human umbelical vein endothelial cells (HUVECs) were divided into normoxic group (21% O

2

)

hypoxia group (1%O

2

) and hypoxia plus NaB trea

tment groups (0

0.3

1 and 3 mmol/L

n=3). A three-gas incubator was used to contain the cells of hypoxia groups

and the cells of normoxic group were cultured in normoxic incubator. The monolayer permeability of HUVECs was tested by Transwell chamber test. Western blotting was performed to detect the protein expression of p120 and β-catenin. The fluorescence intensities of protein p120 and β-catenin were observed by immunofluorescence assay.       Results      The monolayer permeability of HUVECs was significantly higher in the hypoxia groups than the normoxic group (16% vs 10%

P0.05). After addition of 1 mmol/L NaB

the increased monolayer permeability of hypoxia group was inhibited significantly (P0.05). Hypoxia treatment for 12 h induced the protein level of p120 reduced

significantly lower than that of the normoxic group (P0.05)

but hypoxia had no obvious effect on the expression of β-catenin. Hypoxia plus 1 mmol/L NaB treatment promoted the expression of p120 when compared with the simple hypoxia group (P0.05). Immunofluorescence assay showed that the fluorescence intensity of p120 was reduced by hypoxia

but 1 mmol/L NaB reversed this phenomenon.       Conclusion      NaB prevents the hyperpermeability of HUVECs induced by hypoxia

which may be through upregulating p120 protein and thus inhibiting the destruction of the cell adhesion. Therefore NaB inhibits the increase of the permeability of endothelial cells induced by hypoxia.