...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular Neurobiology >The Protective Role of Selenium on Scopolamine-Induced Memory Impairment, Oxidative Stress, and Apoptosis in Aged Rats: The Involvement of TRPM2 and TRPV1 Channels
【24h】

The Protective Role of Selenium on Scopolamine-Induced Memory Impairment, Oxidative Stress, and Apoptosis in Aged Rats: The Involvement of TRPM2 and TRPV1 Channels

机译：硒对龄大鼠Cocopolamine诱导的记忆损伤，氧化应激和细胞凋亡的保护作用：TRPM2和TRPV1通道的累积

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

Inhibition of Ca2+ entry into the hippocampus and dorsal root ganglion (DRG) through inhibition of N-methyl-d-aspartate (NMDA) receptor antagonist drugs is the current standard of care in neuronal diseases such as Alzheimer's disease, dementia, and peripheral pain. Oxidative stress activates Ca2+-permeable TRPM2 and TRPV1, and recent studies indicate that selenium (Se) is a potent TRPM2 and TRPV1 channel antagonist in the hippocampus and DRG. In this study, we investigated the neuroprotective properties of Se in primary hippocampal and DRG neuron cultures of aged rats when given alone or in combination with scopolamine (SCOP). Thirty-two aged (18-24 months old) rats were divided into four groups. The first and second groups received a placebo and SCOP (1 mg/kg/day), respectively. The third and fourth groups received intraperitoneal Se (1.5 mg/kg/ over day) and SCOP + Se, respectively. The hippocampal and DRG neurons also were stimulated in vitro with a TRPV1 channel agonist (capsaicin) and a TRPM2 channel agonist (cumene hydroperoxide). We found that Se was fully effective in reversing SCOP-induced TRPM2 and TRPV1 current densities as well as errors in working memory and reference memory. In addition, Se completely reduced SCOP-induced oxidative toxicity by modulating lipid peroxidation, reducing glutathione and glutathione peroxidase. The Se and SCOP + Se treatments also decreased poly (ADP-ribose) polymerase activity, intracellular free Ca2+ concentrations, apoptosis, and caspase 3, caspase 9, and mitochondrial membrane depolarization values in the hippocampus. In conclusion, the current study reports on the cellular level for SCOP and Se on the different endocytotoxic cascades for the first time. Notably, the research indicates that Se can result in remarkable neuroprotective and memory impairment effects in the hippocampal neurons of rats.
机译：通过抑制N-甲基-D-天冬氨酸（NMDA）受体拮抗剂药物抑制CA2 +进入海马和背根神经节（DRG）是目前神经元疾病如阿尔茨海默病，痴呆和周围疼痛的目前的护理标准。氧化应激激活CA2 + -Permable TRPM2和TRPV1，最近的研究表明，硒（SE）是海马和DRG中的有效的TRPM2和TRPV1通道拮抗剂。在这项研究中，我们在单独给药或与汽油胺（SCOP）组合时，研究了老年大鼠原发性海马和DRG神经元培养物的神经保护性能。三十二岁（18-24个月）大鼠分为四组。第一组和第二组分别接受安慰剂和SCOP（1mg / kg /天）。第三组和第四组分别接受腹膜内培养（1.5mg / kg /次）和scop + se。海马和DRG神经元在体外刺激了TRPV1通道激动剂（辣椒素）和TRPM2通道激动剂（异丙烷氢过氧化物）。我们发现SE完全有效地逆转SCOP引起的TRPM2和TRPV1当前密度以及工作存储器和参考存储器中的错误。此外，通过调节脂质过氧化，还原谷胱甘肽和谷胱甘肽过氧化物酶来完全降低SCOP诱导的氧化毒性。 SE和SCOP + SE治疗还降低了多（ADP-核糖）聚合酶活性，细胞内游离CA2 +浓度，细胞凋亡和半胱天冬酶3，胱天蛋白酶9和线粒体3和线粒体膜去极化值。总之，目前的研究首次研究了SCOP和SE在不同的内胞毒性瀑布上的细胞水平。值得注意的是，研究表明，SE可以导致大鼠海马神经元中的显着神经保护和内存损伤效应。

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