Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells
Protocatechuic acid inhibits apoptosis by mitochondrial dysfunction in rotenone-induced PC12 cells
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DOI：
10.1016/j.tiv.2007.10.012
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发表时间：
2008-03-01
影响因子：
3.2
通讯作者：
An, Li-Jia
中科院分区：
文献类型：
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作者：
Liu, Ye-Ming;Jiang, Bo;An, Li-Jia
原儿茶酸(PCA)是从高良姜仁中分离得到的一种酚类化合物。对过氧化氢(H_2O_2)或MPP+诱导的PC12细胞凋亡有明显的神经保护作用。然而，PCA抑制鱼藤酮诱导的PC12细胞神经毒性的机制尚不清楚。在这项研究中，我们研究了PCA对暴露于鱼藤酮的PC12细胞的保护作用，作为线粒体功能障碍和细胞凋亡的体外模型。鱼藤酮诱导的PC12细胞的凋亡伴随着线粒体膜电位的丧失、活性氧的形成、总谷胱甘肽的耗竭、caspase-3的激活和bcl2的下调。相反，PCA以剂量依赖的方式显著减轻上述线粒体功能障碍。综上所述，这些结果表明，PCA可以通过改善线粒体功能障碍来阻断鱼藤酮诱导的PC12细胞的凋亡。(C)2007爱思唯尔有限公司。保留所有权利。
Protocatechuic acid (PCA), a phenolic compound isolated from the kernels of Alpinia (A.) oxyphylla, showed the significant neuroprotective effects on hydrogen peroxide (H2O2) or MPP+-induced apoptosis in cultured PC12 cells. However, the mechanism how PCA suppresses rotenone-induced neurotoxicity in cultured PC12 cells remains unclear. In this study, we investigated the protective effects of PCA in PC12 cells exposed to rotenone as an in vitro model of mitochondrial dysfunction and apoptotic cell death. The apoptosis in rotenone-induced PC12 cells was accompanied by the loss of mitochondrial membrane potential, the formation of reactive oxygen species (ROS), the total glutathione depletion, activation of caspase-3 and down-regulation of Bcl-2. In contrast, PCA markedly attenuated the above-mentioned mitochondrial dysfunction in a dose-dependent manner. Taken together, these results suggest that treatment of PC12 cells with PCA can block rotenone-induced apoptosis via ameliorating the mitochondrial dysfunction. (C) 2007 Elsevier Ltd. All rights reserved.