...
  • 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 >Chronic social isolation induces NF-κB activation and upregulation of iNOS protein expression in rat prefrontal cortex
【24h】

Chronic social isolation induces NF-κB activation and upregulation of iNOS protein expression in rat prefrontal cortex

机译：慢性社会隔离诱导大鼠前额叶皮层NF-κB活化和iNOS蛋白表达上调

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

Exposure of an organism to stress, results in oxidative stress and increased nitric oxide (NO) production in the brain. The role of the processes caused by chronic stress in the prefrontal cortex has not been fully investigated. Considering that chronic stress increases NO production by the enzyme nitric oxide synthase (NOS), we examined the cytosolic neuronal (nNOS) or inducible (iNOS) protein levels in the prefrontal cortex of rats exposed to 21 d of chronic social isolation stress, an animal model of depression, alone or in combination with 2 h of acute immobilization or cold (4 °C) stress (combined stress). Antioxidative status via cytosolic CuZnSOD and mitochondrial MnSOD activity, cytosolic redox status via reduced glutathione (GSH) concentration were determined. Furthermore, cytosolic inducible heat shock protein 70 (Hsp70i), cytosolicuclear distributions of NF-κB and serum corticosterone (CORT) were also investigated to elucidate the possible mechanism involved in the cellular NOS pathway. Our results showed that both acute stressors led to increases of CORT and nNOS protein while iNOS protein expression was unaffected. In contrast to the acute stress, chronic social isolation compromised hypothalamic- pituitary-adrenal axis functioning such that the normal stress response was impaired following subsequent acute stressors. Downregulated redox GSH status as well as decreased activity of CuZnSOD and MnSOD suggests the existence of oxidative stress which remained as such following combined stressors. Changes in redox-status associated with decreased Hsp70i protein expression enabled NF-κB translocation into the nucleus, causing increased cytosolic nNOS and iNOS protein expression. Results suggest that NOS signaling pathway plays a differential role between acute and chronic stress whereby state of oxidative/ nitrosative stress after chronic social isolation is caused, at least in part, by NF-κB activation and increased iNOS protein expression.
机译：生物体承受压力会导致氧化应激并增加大脑中一氧化氮（NO）的产生。由慢性压力在前额叶皮层中引起的过程的作用尚未得到充分研究。考虑到慢性应激会增加一氧化氮合酶（NOS）产生的NO的产生，我们研究了暴露于21 d慢性社交隔离应激的大鼠（动物）前额叶皮层中的胞浆神经元（nNOS）或诱导型（iNOS）蛋白水平单独或与2小时的急性固定或冷（4°C）应激（合并应激）结合使用时的抑郁模型。确定了通过胞质CuZnSOD的抗氧化状态和线粒体MnSOD活性，通过降低谷胱甘肽（GSH）浓度的胞质氧化还原状态。此外，还研究了胞质诱导性热休克蛋白70（Hsp70i），NF-κB的胞质/核分布和血清皮质酮（CORT），以阐明参与细胞NOS途径的可能机制。我们的结果表明，两种急性应激源均导致CORT和nNOS蛋白增加，而iNOS蛋白表达未受影响。与急性应激相反，慢性社会隔离损害了下丘脑-垂体-肾上腺轴功能，以致随后的急性应激后正常应激反应受到损害。氧化还原谷胱甘肽状态的下调以及CuZnSOD和MnSOD活性的降低表明存在氧化应激，该氧化应激在组合应激源后仍保持不变。与Hsp70i蛋白表达降低相关的氧化还原状态变化使NF-κB易位进入细胞核，导致胞质nNOS和iNOS蛋白表达增加。结果表明，NOS信号通路在急性和慢性应激之间起着不同的作用，由此慢性社会隔离后的氧化/亚硝化应激状态至少部分是由NF-κB活化和iNOS蛋白表达增加引起的。

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