The Neuroprotective Effects of Decursin Isolated from Angelica gigas Nakai Against Amyloid β-Protein-Induced Apoptosis in PC 12 Cells via a Mitochondria-Related Caspase Pathway
The Neuroprotective Effects of Decursin Isolated from Angelica gigas Nakai Against Amyloid β-Protein-Induced Apoptosis in PC 12 Cells via a Mitochondria-Related Caspase Pathway
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DOI：
10.1007/s11064-015-1623-0
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发表时间：
2015-08-01
影响因子：
4.4
通讯作者：
Lee, Yongwoo
中科院分区：
文献类型：
--
作者：
Li, Li;Du, Jikun;Lee, Yongwoo
从当归中提纯的Decursin已被证明具有神经保护作用。先前的研究表明，decursin保护PC 12细胞免受A β（25-35）诱导的氧化细胞毒性。本研究旨在探讨decursin对A β诱导的PC 12细胞凋亡的保护作用。我们的结果表明，decursin预处理的PC 12细胞显着抑制A β（25-35）诱导的细胞毒性和凋亡。其作用机制可能是逆转A β（25-35）诱导的线粒体功能障碍，包括降低线粒体膜电位、抑制活性氧产生、减少PC 12细胞中线粒体释放细胞色素c。此外，decursin显著抑制caspase-3的活性，并调节A β诱导的Bcl-2/Bax的比例（25-35）。这些发现表明，decursin对A β（25-35）诱导的PC 12细胞神经毒性发挥神经保护作用，至少部分是通过抑制细胞凋亡的线粒体途径。
Decursin, purified from Angelica gigas Nakai, has been proven to exert neuroprotective property. Previous study revealed decursin protected the PC12 cells from A beta(25-35)-induced oxidative cytotoxicity. The present study aimed to investigate whether decursin could protect PC12 cells from apoptosis caused by A beta. Our results indicated that pretreatment of PC12 cells with decursin significantly inhibited A beta(25-35)-induced cytotoxicity and apoptosis. The mechanism of action is likely to reverse A beta(25-35)-induced mitochondrial dysfunction, including the reduction of mitochondrial membrane potential, the inhibition of reactive oxygen species production, and the decrease of mitochondrial release of cytochrome c in PC12 cells. In addition, decursin significantly suppressed the activity of caspase-3 and moderated the ratio of Bcl-2/Bax induced by A beta(25-35). These findings indicate that decursin exerts a neuroprotective effect against A beta(25-35)-induced neurotoxicity in PC12 cells, at least in part, via suppressing the mitochondrial pathway of cellular apoptosis.