首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Electroacupuncture Could Regulate the NF-rB Signaling Pathway to Ameliorate the Inflammatory Injury in Focal Cerebral Ischemia/Reperfusion Model Rats
【24h】

Electroacupuncture Could Regulate the NF-rB Signaling Pathway to Ameliorate the Inflammatory Injury in Focal Cerebral Ischemia/Reperfusion Model Rats

机译:电针对局灶性脑缺血再灌注模型大鼠炎症损伤的NF-rB信号通路调控。

获取原文
获取原文并翻译 | 示例
           

摘要

The activated nuclear factor-KappaB signaling pathway plays a critical role in inducing inflammatory injury. It has been reported that electroacupuncture could be an effective anti-inflammatory treatment. We aimed to explore the complex mechanism by which EA inhibits the activation of the NF-kB signal pathway and ameliorate inflammatory injury in the short term; the effects of NEMO Binding Domain peptide for this purpose were compared. Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 hrs. Total 380 male Sprague-Dawley rats are in the study. The neurobehavioral scores, infarction volumes, and the levels of IL-1beta and IL-13 were detected. NF-kappaB p65, IkappaBalpha, IKKalpha, and IKKbeta were analyzed and the ability of NF-kappaB binding DNA was investigated. The EA treatment and the NBD peptide treatment both reduced infarct size, improved neurological scores, and regulated the levels of IL-1beta and IL-13. The treatment reduced the expression of IKKalpha and IKKbeta and altered the expression of NF-kappaB p65 and IkappaBalpha in the cytoplasm and nucleus; the activity of NF-kB was effectively reduced. We conclude that EA treatment might interfere with the process of NF-kB nuclear translocation. And it also could suppress the activity of NF-kB signaling pathway to ameliorate the inflammatory injury after focal cerebral ischemia/reperfusion.
机译:激活的核因子-KappaB信号通路在诱导炎症损伤中起关键作用。据报道,电针可能是一种有效的消炎治疗方法。我们的目的是探索一种复杂的机制,EA可以在短期内抑制NF-kB信号通路的激活并减轻炎性损伤。比较了NEMO结合域肽为此目的的效果。大脑中动脉闭塞2小时可诱发局灶性脑I / R。总共380只雄性Sprague-Dawley大鼠正在研究中。检测神经行为评分,梗死体积以及IL-1beta和IL-13的水平。分析了NF-kappaB p65,IkappaBalpha,IKKalpha和IKKbeta,并研究了NF-kappaB结合DNA的能力。 EA治疗和NBD肽治疗均能减少梗塞面积,改善神经功能评分并调节IL-1beta和IL-13的水平。该处理降低了IKKalpha和IKKbeta的表达,并改变了细胞质和细胞核中NF-kappaB p65和IkappaBalpha的表达。 NF-kB的活性被有效降低。我们得出的结论是,EA治疗可能会干扰NF-kB核易位的过程。并且它还可以抑制NF-kB信号通路的活性,以减轻局灶性脑缺血/再灌注后的炎症损伤。

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