4.7 Article

Baicalein protects Human melanocytes from H2O2-induced apoptosis via inhibiting mitochondria-dependent caspase activation and the p38 MAPK pathway

期刊

FREE RADICAL BIOLOGY AND MEDICINE
卷 53, 期 2, 页码 183-193

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2012.04.015

关键词

Baicalein; Melanocyte; Apoptosis; Mitochondrion; Hydrogen peroxide; Oxidative stress; Vitiligo

资金

  1. National Natural Science Foundation of China [81102669, 30972642, 30972528, 81000701, 81130032]
  2. Post-doctoral Science Foundation of China [20100481472]

向作者/读者索取更多资源

The removal of H2O2 by antioxidants has been proven to be beneficial to patients with vitiligo. Baicalein (5,6,7-trihydroxyflavone; BE) has antioxidant activity and has been used in vitiligo therapy in Chinese traditional medicine. In this study, we investigated the potential protective effect and mechanisms of BE against H2O2-induced apoptosis in human melanocytes. Melanocytes from the PIG1 cell line were pretreated with different concentrations of BE for 1 h, followed by exposure to 1.0 mM H2O2 for 24 h. Cell apoptosis, reactive oxygen species levels, and mitochondrial membrane potentials were evaluated by flow cytometry, and cell viability was determined by an MTT assay. The expressions of Bax, Bcl-2, caspase-3, total and phosphorylated ERKs, and p38 MAPK were assayed by Western blot to investigate the possible molecular mechanisms. Our results showed that BE significantly inhibited H2O2-induced apoptosis, intracellular reactive oxygen species generation, and changes in the mitochondrial membrane potential. It also reduced the Bax/Bcl-2 ratio, the release of cytochrome c, the activation of caspase-3, and the phosphorylation of p38 MAPK in a concentration-dependent manner. The results demonstrate for the first time that BE exerts a cytoprotective role in H2O2-induced apoptosis by inhibiting the mitochondria-dependent caspase activation and p38 MAPK pathway. (C) 2012 Elsevier Inc. All rights reserved.

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