The aim of this study was to investigate the effect of resveratrol on the oxidative stress-induced inhibition of gap junctional intercellular communication in HaCaT keratinocytes. Anti-oxidative activity of resveratrol was measured by $alpha,alpha$-diphenyl-$eta$-picrylhydrazyl assay and dichlorodihydrofluorescein diacetate oxidation assay. Gap junctional intercellular communication in HaCaT keratinocytes was assessed using the scrape loading/dye transfer technique. Western blots and reverse transcription-polymerase chain reaction were also analyzed for connexin 43 protein and mRNA expression, respectively. Resveratrol scavenged directly the stable $alpha,alpha$-diphenyl-$eta$-picrylhydrazyl radical over a concentration range of 4 mg/ml ($78.2{pm}2.7$% of control) to 500 mg/ml ($29.9{pm}4.2$% of control) and decreased the intracellular reactive oxygen species induced by ultraviolet A (UVA) irradiation ($89.3{pm}1.1$% of UVA group), ultraviolet B (UVB) irradiation ($70.9{pm}1.7$% of UVB group) and 12-0-tet-radecanoylphorbol-13-acetate (TPA, $48.3{pm}1.1$% of TPA group), respectively. UVA irradiation and TPA markedly reduced gap junctional intercellular communication, which was restored by resveratrol. There were no significant differences in the level of connexin 43 protein and mRNA expression among any of the experimental groups. Our data suggests that resveratrol has the protective effect on the oxidative stress-induced inhibition of gap junctional intercellular communication in HaCaT keratinocytes, and this protection is likely due to the scavenging of reactive oxygen species.