• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Inhibition of glutathione depletion by retinoic acid and tocopherol protects cultured neurons from staurosporine-induced oxidative stress and apoptosis.
【24h】

Inhibition of glutathione depletion by retinoic acid and tocopherol protects cultured neurons from staurosporine-induced oxidative stress and apoptosis.

机译：维甲酸和生育酚对谷胱甘肽耗竭的抑制作用可保护培养的神经元免受星形孢菌素诱导的氧化应激和细胞凋亡的影响。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Cellular redox status is an important factor during neuronal apoptosis. In primary cultures of chick embryonic neurons, serum deprivation and treatment with staurosporine (200 nM) for 24 h increased the percentage of apoptotic neurons from 13% in controls to 28%, and 68%, respectively. Both exposure to staurosporine and serum deprivation resulted in a four-fold increase in the mitochondrial reactive oxygen species production 4 h after the onset of the injury. Whereas the intracellular glutathione content remained unchanged by serum deprivation, it was markedly reduced by staurosporine suggesting that an increased reactive oxygen species production was more deleterious at a low intracellular glutathione content. Treatment with L-buthionine-(S,R)-sulfoximine, an inhibitor of the glutathione synthesis, decreased the intracellular glutathione content, but did not significantly alter the percentage of apoptotic neurons. Tocopherol (10 microM) and retinoic acid (0.1 microM) inhibited staurosporine-induced glutathione depletion as well as the increase in the percentage of apoptotic neurons. We conclude that under conditions of an increased reactive oxygen species production a high intracellular glutathione content could protect neurons from apoptotic injury and that drugs inhibiting the glutathione depletion could prevent neurons from oxidative damage.
机译：细胞氧化还原状态是​​神经元凋亡过程中的重要因素。在鸡胚神经元的原代培养中，血清剥夺和星形孢菌素（200 nM）处理24小时可使凋亡神经元的百分比从对照组的13％分别增加到28％和68％。暴露于星形孢菌素和血清剥夺都导致损伤发作后4小时线粒体活性氧的产生增加了四倍。血清剥夺后细胞内谷胱甘肽含量保持不变，但星形孢菌素显着降低了谷胱甘肽含量，这表明在细胞内谷胱甘肽含量低的情况下，增加的活性氧产生更为有害。用谷胱甘肽合成抑制剂L-buthionine-（（S，R）-sulfoximine）处理可降低细胞内谷胱甘肽含量，但不会显着改变凋亡神经元的百分比。生育酚（10 microM）和视黄酸（0.1 microM）抑制星形孢菌素诱导的谷胱甘肽耗竭以及凋亡神经元百分比的增加。我们得出结论，在增加活性氧产生的条件下，高细胞内谷胱甘肽含量可以保护神经元免受细胞凋亡损伤，而抑制谷胱甘肽耗竭的药物可以防止神经元受到氧化损伤。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号