Wnt3a protects melanocytes iMC65 against oxidative stress
- VernacularTitle:Wnt3a减轻黑素细胞iMC65氧化应激损伤
- Author:
Yan ZHENG
1
;
Ke YANG
;
sha Ya LI
;
fang Shi DONG
;
na Li ZHOU
Author Information
1. 重庆医科大学附属儿童医院儿科研究所 儿童发育疾病研究教育部重点实验室 儿童发育重大疾病国家国际科技合作基地重庆市干细胞治疗工程技术研究中心
- Keywords:
Wnt3a;
melanocyte;
Nrf2;
oxidative stress
- From:
Basic & Clinical Medicine
2017;37(10):1389-1394
- CountryChina
- Language:Chinese
-
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,H2O2treatment group,Wnt3a treatment group.The melanocytes were treated with 750 μmol/L H2O2for 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 microscopy 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 Western blot. Results Compared with control group,cell activity decreased(P<0.01),the ratio of apoptosis increased(P<0.01),ROS production was raised in H2O2treatment group(P<0.01). While compared with H2O2treatment group,cell activity was relieved(P<0.05), the ratio of apoptosis decreased(P<0.05), ROS production was de-clined 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. Conclusions Wnt3a protects the melanocytes against oxi-dative injury by H2O2. The mechanism would be related to the activation of Nrf2/ARE pathway.
