秋水仙碱诱导的 PC12 细胞凋亡被糖原合酶激酶-3 抑制剂所阻止。
Colchicine-induced apoptosis was prevented by glycogen synthase kinase-3 inhibitors in PC12 cells.
机构信息
Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.
出版信息
Cell Mol Neurobiol. 2010 Aug;30(6):863-8. doi: 10.1007/s10571-010-9514-z. Epub 2010 Mar 19.
Abstract
The purpose of this study was to examine whether glycogen synthase kinase-3 (GSK-3) is involved in colchicine-induced cell death in PC12 cells by using GSK inhibitors. Colchicine increased apoptotic cell death with morphological changes characterized by cell shrinkage and nuclear condensation or fragmentation. GSK-3 inhibitors such as alsterpaullone, SB216763, and AR-A014418 prevented colchicine-induced cell death and caspase-3 activation. These results suggest that colchicine induces caspase-dependent apoptotic cell death and that GSK-3 activation is involved in cell death in PC12 cells.
摘要
本研究旨在通过使用 GSK 抑制剂来检测糖原合酶激酶-3（GSK-3）是否参与秋水仙碱诱导的 PC12 细胞死亡。秋水仙碱增加了凋亡细胞死亡，其形态特征为细胞收缩和核浓缩或碎裂。GSK-3 抑制剂如 alsterpaullone、SB216763 和 AR-A014418 可防止秋水仙碱诱导的细胞死亡和 caspase-3 激活。这些结果表明，秋水仙碱诱导 caspase 依赖性凋亡细胞死亡，而 GSK-3 的激活参与了 PC12 细胞的死亡。
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