| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10738037 | Free Radical Biology and Medicine | 2012 | 11 Pages |
Abstract
⺠We investigated the role and mechanisms of BE in H2O2-induced melanocyte apoptosis. ⺠BE inhibited H2O2-induced oxidative stress and mitochondrial-dependent apoptosis. ⺠BE inhibited H2O2-induced p38 MAPK phosphorylation but had no effect on ERKs. ⺠Inhibition of caspase and p38 MAPK pathways abolished the cytoprotective role of BE. ⺠BE exerts a cytoprotective role through inhibiting caspase and p38 MAPK pathways.
Keywords
Tris buffer solutionBcl-2TBSbaicaleinERKPVDFJnkDMEMPBSc-Jun N-terminal kinaseDMSOMAPKDulbecco's modified Eagle's mediumMTTROSHydrogen peroxideBaxOxidative stressApoptosispolyvinylidene difluorideDimethyl sulfoxidelactate dehydrogenaseLDHB cell lymphoma 2phosphate buffer solutionMelanocyteMitochondrionmitogen-activated protein kinasevitiligoextracellular signal-regulated kinaseReactive oxygen species
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Authors
Bangmin Liu, Zhe Jian, Qiang Li, Kai Li, Zhiyong Wang, Ling Liu, Lingzhen Tang, Xiuli Yi, Hua Wang, Chunying Li, Tianwen Gao,