Liu Ye-Ming, Jiang Bo, Bao Yong-Ming, An Li-Jia
Department of Bioscience and Biotechnology, Dalian University of Technology, Dalian 116024, China.
Toxicol In Vitro. 2008 Mar;22(2):430-7. doi: 10.1016/j.tiv.2007.10.012. Epub 2007 Nov 7.
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.
原儿茶酸(PCA)是从益智仁中分离出的一种酚类化合物,对过氧化氢(H2O2)或MPP +诱导的PC12细胞凋亡具有显著的神经保护作用。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。在本研究中,我们以鱼藤酮诱导的线粒体功能障碍和凋亡细胞死亡的体外模型,研究了PCA对PC12细胞的保护作用。鱼藤酮诱导的PC12细胞凋亡伴随着线粒体膜电位的丧失、活性氧(ROS)的形成、总谷胱甘肽的消耗、caspase-3的激活以及Bcl-2的下调。相比之下,PCA以剂量依赖的方式显著减轻了上述线粒体功能障碍。综上所述,这些结果表明,用PCA处理PC12细胞可以通过改善线粒体功能障碍来阻断鱼藤酮诱导的细胞凋亡。