...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Leptin induces cyclooxygenase-2 via an interaction with interleukin-1beta in the rat brain.
【24h】

Leptin induces cyclooxygenase-2 via an interaction with interleukin-1beta in the rat brain.

机译：瘦素通过与大鼠脑中白介素-1β的相互作用诱导环氧合酶-2。

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

In addition to its central effects on appetite regulation, leptin has been implicated in immune function and inflammation. Previous data suggested that leptin acts as an inflammatory signal within the brain, as exogenously administered leptin induced fever, a typical brain-regulated inflammatory response. The present study aimed to delineate the inflammatory actions and cellular targets of leptin in the brain by examining its effects on the expression of interleukin (IL)-1beta and cyclooxygenase (COX)-2, two important inflammatory components of the fever response. Intracerebroventricular injection of leptin (5 microg/rat) induced IL-1beta and COX-2 mRNA and protein in the hypothalamus between 1 and 3 h after treatment as determined by reverse transcription-polymerase chain reaction and immunohistochemistry. Coinjection of IL-1 receptor antagonist (100 microg/rat, intracerebroventricular) attenuated leptin-induced COX-2, whereas IL-1 receptor antagonist had no effect on endogenous IL-1beta levels, suggesting that leptin induces COX-2 via, at least partly, IL-1beta action. IL-1beta protein expression was induced in macrophages in the meningis and perivascular space after leptin treatment, whereas COX-2 induction was observed in endothelial cells, indicating the roles for these non-neuronal cells in mediating inflammatory actions of leptin. In addition, neutralization of endogenous circulating leptin with anti-leptin antiserum attenuated intraperitoneal lipopolysaccharide (100 microg/kg)-induced brain IL-1beta and COX-2 upregulation, suggesting that leptin indeed acts as an inflammatory signal to the brain during systemic inflammation. These findings are in contrast to the effects of leptin on appetite regulation where it is believed to act primarily on neurons, thus presenting a distinct anatomical basis for the inflammatory and appetite regulatory actions of leptin in the brain.
机译：除了对食欲调节的主要作用外，瘦素还与免疫功能和炎症有关。先前的数据表明，瘦素可作为外源性瘦素引起的发烧（一种典型的大脑调节性炎症反应），在大脑内充当炎症信号。本研究旨在通过检查瘦素对发烧反应的两个重要炎症成分白介素（IL）-1β和环氧合酶（COX）-2表达的影响来描述脑中瘦素的炎性作用和细胞靶标。经逆转录-聚合酶链反应和免疫组化测定，脑室内注射瘦素（5微克/大鼠）可在治疗后1至3小时内诱导下丘脑IL-1beta和COX-2 mRNA和蛋白质。共注射IL-1受体拮抗剂（100微克/大鼠，脑室内）减弱了瘦素诱导的COX-2，而IL-1受体拮抗剂对内源性IL-1beta水平没有影响，这表明瘦素至少通过以下方式诱导COX-2：部分是IL-1beta的作用。瘦素处理后，在脑膜和血管周围空间的巨噬细胞中诱导了IL-1β蛋白的表达，而在内皮细胞中观察到了COX-2的诱导，表明这些非神经细胞在介导瘦素的炎症作用中发挥了作用。此外，用抗瘦素抗血清中和内源性循环瘦素可减轻腹膜内脂多糖（100 microg / kg）诱导的大脑IL-1beta和COX-2上调，表明瘦素确实在全身性炎症期间充当了大脑的炎症信号。这些发现与瘦素对食欲调节的作用相反，瘦素被认为主要作用于神经元，因此为瘦素在大脑中的炎症和食欲调节作用提供了独特的解剖学基础。

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