• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cytokine >Soluble A beta(1-42) suppresses TNF-alpha and activates NLRP3 inflammasome in THP-1 macrophages
【24h】

Soluble A beta(1-42) suppresses TNF-alpha and activates NLRP3 inflammasome in THP-1 macrophages

机译：可溶性β（1-42）抑制TNF-α，并在THP-1巨噬细胞中激活NLRP3炎症

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

Deposition of amyloid-beta in Alzheimer's disease is accompanied by chronic inflammation, which involves raised levels of pro-inflammatory cytokines TNF-alpha, IL-6 and IL-1 beta. However, the role of A beta(1-42) in the inflammatory process, before it gets deposited into aggregates has not been investigated thoroughly. Through this study, we are illustrating the dual role of soluble A beta(1-42) (sA beta(1-42)) in activating the NLRP3 inflammasome and simultaneously inhibiting TNF-alpha secretion. Our data suggested that the treatment of chronically induced THP-1 macrophages and N9 microglial cells with sA beta(1-42) can suppress the major inflammatory cytokine TNF-alpha without affecting the level of IL-6. However, the activation of NLRP3 inflammasome was well evidenced by secretion of IL-1 beta, increased expression of NLRP3 and caspase-1, implicating sA beta(1-42) in enhancing and suppressing one or other type of inflammation. Further investigation revealed that sA beta(1-42) was able to severely abrogate the expression of NF-kappa B, p50 and restricting the translocation of NF-kappa B, p65 to nucleus by inhibiting phosphorylation of I kappa B-alpha in THP-1 macrophages. These data indicate that the sA beta(1-42) may play a dual role during inflammatory process, wherein, it may be involved in protecting the cells from inflammatory damage due to TNF-alpha. This ability of sA beta(1-42) might be playing some role in protecting the brain cells during the process of aging and Alzheimer's disease, where, chronic inflammatory environment plays a vital role.
机译：在阿尔茨海默病的疾病中沉积淀粉样蛋白β伴有慢性炎症，其涉及募集水平的促炎细胞因子TNF-α，IL-6和IL-1β。然而，β（1-42）在炎症过程中的作用尚未彻底调查炎症过程之前。通过该研究，我们正在溶解β（1-42）（SAβ（1-42））在激活NLRP3炎性和同时抑制TNF-α分泌时的双重作用。我们的数据表明，使用SAβ（1-42）的慢性诱导的THP-1巨噬细胞和N9微胶质细胞的治疗可以抑制主要炎症细胞因子TNF-α，而不会影响IL-6水平。然而，通过IL-1β的分泌，NLRP3和Caspase-1的表达增加，含有SAβ（1-42）的增强和抑制一种或其他类型的炎症来迅速地证明NLRP3炎性炎性炎症组的激活。进一步的研究表明，SAβ（1-42）能够严重消除NF-Kappa B，P50的表达，并通过抑制THP-磷酸盐的磷酸化来限制NF-Kappa B，P65对核的易位。 1巨噬细胞。这些数据表明SAβ（1-42）可以在炎症过程中发挥双重作用，其中，它可以参与保护细胞免受TNF-α引起的炎性损伤。 SAβ（1-42）的这种能力可能在衰老过程中保护脑细胞和阿尔茨海默病过程中的作用，在那里，慢性炎症环境起着至关重要的作用。

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