Baicalein protects Human melanocytes from H2O2-induced apoptosis via inhibiting mitochondria-dependent caspase activation and the p38 MAPK pathway
Baicalein protects Human melanocytes from H2O2-induced apoptosis via inhibiting mitochondria-dependent caspase activation and the p38 MAPK pathway
复制标题
黄芩素通过抑制线粒体依赖性 caspase 激活和 p38 MAPK 通路，保护人黑素细胞免受 H2O2 诱导的细胞凋亡
DOI：
10.1016/j.freeradbiomed.2012.04.015
复制
发表时间：
2012-07-15
影响因子：
7.4
通讯作者：
Gao, Tianwen
中科院分区：
文献类型：
--
作者：
Liu, Bangmin;Jian, Zhe;Gao, Tianwen
通过抗氧化剂去除H2 O2已被证明对白癜风患者有益。黄芩素（5，6，7-三羟基黄酮; BE）具有抗氧化活性，已被用于白癜风的中医治疗。在这项研究中，我们探讨了潜在的保护作用和BE对H2 O2诱导的人黑素细胞凋亡的机制。用不同浓度的BE预处理PIG 1细胞系的黑素细胞1 h，然后暴露于1.0 mM H2 O2 24 h。细胞凋亡，活性氧水平，线粒体膜电位通过流式细胞术进行了评价，并通过MTT法测定细胞活力。Western blot检测Bax、Bcl-2、caspase-3、总ERK和磷酸化ERK以及p38 MAPK的表达，探讨其可能的分子机制。我们的研究结果表明，BE显着抑制过氧化氢诱导的细胞凋亡，细胞内活性氧的产生，并在线粒体膜电位的变化。它还以浓度依赖性方式降低Bax/Bcl-2比值、细胞色素c释放、caspase-3活化和p38 MAPK磷酸化。结果首次证明BE通过抑制H_2O_2诱导的细胞凋亡的caspase激活和p38 MAPK通路发挥细胞保护作用。(C)2012 Elsevier Inc. All rights reserved.
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.