首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Electroacupuncture Could Regulate the NF-κB Signaling Pathway to Ameliorate the Inflammatory Injury in Focal Cerebral Ischemia/Reperfusion Model Rats
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Electroacupuncture Could Regulate the NF-κB 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-κB信号通路的调节。

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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-κB 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-1βand IL-13 were detected. NF-κB p65, IκBα, IKKα, and IKKβwere analyzed and the ability of NF-κB 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-1βand IL-13. The treatment reduced the expression of IKKαand IKKβand altered the expression of NF-κB p65 and IκBαin the cytoplasm and nucleus; the activity of NF-κB was effectively reduced. We conclude that EA treatment might interfere with the process of NF-κB nuclear translocation. And it also could suppress the activity of NF-κB signaling pathway to ameliorate the inflammatory injury after focal cerebral ischemia/reperfusion.
机译:活化的核因子-KappaB信号通路在诱导炎症损伤中起关键作用。据报道,电针可以是一种有效的消炎治疗方法。我们的目的是探索复杂的机制,EA可以在短期内抑制NF-κB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。局灶性脑I / R是由大脑中动脉闭塞2小时引起的。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-1β和IL-13的水平。分析了NF-κBp65,IκBα,IKKα和IKKβ,并研究了NF-κB结合DNA的能力。 EA治疗和NBD肽治疗均能减少梗死面积,改善神经功能评分并调节IL-1β和IL-13的水平。该处理降低了细胞质和细胞核中IKKα和IKKβ的表达,并改变了NF-κBp65和IκBα的表达。有效降低了NF-κB的活性。我们得出结论,EA治疗可能会干扰NF-κB核移位的过程。并且它还可以抑制NF-κB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。

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