Objective       To determine the effect of resveratrol on high glucose-induced epithelia-mesenchymal transit

ion (EMT) of renal tubular epithelial cell line HK-2 and its underlying mechanism.       Methods         Cultured HK-2 cells were divided into 6 groups

that is

normal glucose (NG

5.5 mmol/L)

high glucose (HG

30 mmol/L)

resveratrol (RES

10 μmol/L)

high glucose and resveratrol (HG+RES

30 mmol/L + 10 μmol/L)

diphenyleneiodonium (DPI

NADPH oxdiase inhibitor

10 μmol/L)

and high glucose and DPI group (HG+DPI

30 mmol/L + 10 μmol/L). Inverted microscopy was used to observe the morphological changes in high glucose-induced HK-2 cells. Expression of cytokeratin and vimentin was detected by immunofluorescence assay

and that of of α-smooth muscle actin (α-SMA)

E-cadherin

NADPH oxdiase subunits (NOXs) were measured by Western blotting. Intracellular reactive oxide species (ROS) were detected by DCFH-DA fluorescence probe.       Results         After incubated with high glucose

HK-2 cells turned into long spindle-shape compared with NG group. Protein levels of epithelial markers E-cadherin and cytokeratin were significantly decreased

while those of the mesenchymal markers α-SMA and vimentin were increased (

P

0.01). Protein levels of NADPH oxidase subunits NOX1 and NOX4 were significantly decreased (

P

0.01)

but that of NOX2 had no change

and intracellular ROS production was significantly increased (1 723.82±303.97 vs 2 579.36±353.76

P

0.01). The pre-incubation of resveratrol or DPI obviously inhibited EMT (

P

0.01) and ROS production (1 803.36±199.54 and 1 837.45±266.83 vs 2 579.36±353.76

P

0.01) in HK-2cells induced by high glucose

while resveratrol markedly inhibited NOX1 and NOX4 expression (

P

0.01).       Conclusion         Resveratrol may reduce ROS production through suppressing NADPH oxidase in renal epithelial cells

and thus inhibit the EMT of the cells induced by high glucose.