Abstract: Objective To investigate the protective effect of Wnt3a on the oxidative stress damage of melanocytes and its mechanism. Methods The melanocytes were divided into 4 groups: control group, Wnt3a group, H2O2 treatment group, Wnt3a treatment group. The melanocytes were treated with 750 μmol/L H2O2 for oxidative stress damage. The activity of cells was detected by MTT assay. The apoptosis rate was examined by flow cytometry. The ROS production was observed by fluorescence microscope and flow cytometry. The Nrf2/ARE pathway activation was determined with an ARE-driven luciferase reporter construct. The expressions of Nrf2 and HO-1 were examined by Westernblot. Results Compared with control group, cell activity was decreased（p<0.01）, the ratio of apoptosis was increased（p<0.01）, ROS production was raised in H2O2 treatment group（p<0.01）. While compared with H2O2 treatment group, cell activity was relieved（p<0.05）, the ratio of apoptosis was decreased（p<0.05）, ROS production was declined in Wnt3a treatment group（p<0.05）.Wnt3a up-regulated the transcriptional activity of Nrf2 as determined with improving the relative activity of luciferase regulated by the antioxidant response element ARE. Wnt3a also increases the expression of Nrf2 and HO-1 protein levels. Conclusion Wnt3a protects the melanocytes against oxidative injury by H2O2. The mechanism would be related to the activation of Nrf2/ARE pathway.

Key words: Wnt3a, melanocyte, Nrf2, oxidative stress