Abstract

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-1β and IL-13 were detected. NF-κB p65, IκBα, IKKα, and IKKβ were 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-1β and IL-13. The treatment reduced the expression of IKKα and IKKβ and altered the expression of NF-κB p65 and IκBα in 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.

Highlights

  • The pathological mechanism of focal cerebral ischemia/reperfusion is very complex and involves a myriad of distinct molecular signaling and cytokines pathways [1]

  • The effect in NBD group was more remarkable than that in EA group (P < 0.05) (Figure 1). These results suggested that EA treatment and NBD treatment both ameliorated the neurologic deficit symptoms caused by I/R and promoted the movement recovery degree

  • The EA treatment regulated the levels of interleukin (IL-1β and IL-13) in brain and serum after focal cerebral I/R

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Summary

Introduction

The pathological mechanism of focal cerebral ischemia/reperfusion is very complex and involves a myriad of distinct molecular signaling and cytokines pathways [1]. Inflammation is a pathological process that occurs via an amplification cascade, the NF-κB signaling pathway [5], and the complex cytokine network is critical for the occurrence of inflammatory responses [6, 7]. More sophisticated approaches are required for the treatment of focal cerebral ischemia/reperfusion because of the narrow therapeutic time window and complex pathological features of this disease [8]. The mechanism by which EA suppresses the activity of NF-κB signaling pathway at an early stage of cerebral ischemia/reperfusion needs to be discussed

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