Electroacupuncture pretreatment ameliorates cerebral ischemia/reperfusion injury by inhibiting the miR-124/NF-κB/Fas signaling pathway.

IF 1.7 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2025-10-01 Epub Date: 2025-09-01 DOI:10.1097/WNR.0000000000002211

Junli Wang, Lida Zhang, Suwen Li, Tingting Tong, Chenglong Li, Haisheng Ji, Junyu Zhang, Kuiwu Li, Xiaoge Song, Wei Han, Ying Wang

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Abstract

Background: The mechanism of electroacupuncture (EA) pretreatment for cerebral ischemia-reperfusion injury (CIRI) is unclear. This study aimed to investigate whether EA pretreatment attenuates CIRI through the miR-124/nuclear factor kappa B (NF-κB)/Fas signaling pathway.

Methods: Following 7 days of EA pretreatment at Baihui (GV20), Fengfu (GV16), and Dazhui (GV14), CIRI rats were established. Neuroprotection was assessed using modified neurological severity score (mNSS), 2,3,5-triphenyltetrazolium chloride staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Neuronal ultrastructure was examined by electron microscopy. Immunofluorescence staining revealed pNF-κB and Fas expression patterns. Western blotting and real-time quantitative PCR were employed to quantify miR-124, NF-κB repressing factor (NKRF), pNF-κB/NF-κB ratio, Fas, FasL, fas-associated protein with death domain (FADD), caspase-3, and caspase-8 in the cerebral cortex.

Results: EA pretreatment reduced cerebral infarction volume, alleviated mNSS and cortical neuronal apoptosis. Moreover, EA pretreatment downregulated miR-124, pNF-κB/NF-κB/Fas, FasL, FADD levels and increased NKRF expression. The effect of EA pretreatment was enhanced by miR-124 inhibitor.

Conclusion: These findings suggest that EA pretreatment attenuated neuronal apoptosis through suppression of the miR-124/NF-κB/Fas signaling pathway in CIRI.

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电针预处理通过抑制miR-124/NF-κB/Fas信号通路改善脑缺血再灌注损伤。

背景：电针预处理治疗脑缺血再灌注损伤（CIRI）的机制尚不清楚。本研究旨在探讨EA预处理是否通过miR-124/核因子κB (NF-κB)/Fas信号通路减弱CIRI。方法：以百会（GV20）、丰复（GV16）、大椎（GV14）预处理7 d，建立CIRI大鼠。采用改良神经系统严重程度评分（mNSS）、2,3,5-三苯四唑氯染色和末端脱氧核苷酸转移酶dUTP缺口端标记染色评估神经保护作用。电镜观察神经元超微结构。免疫荧光染色显示pNF-κB和Fas的表达模式。采用Western blotting和实时荧光定量PCR技术，定量小鼠大脑皮层miR-124、NF-κB抑制因子（NKRF）、pNF-κB/NF-κB比值、Fas、FasL、Fas相关死亡结构域蛋白（FADD）、caspase-3、caspase-8。结果：EA预处理可减少脑梗死体积，减轻mNSS和皮质神经元凋亡。此外，EA预处理下调miR-124、pNF-κB/NF-κB/Fas、FasL、FADD水平，增加NKRF表达。miR-124抑制剂可增强EA预处理的效果。结论：上述结果提示EA预处理通过抑制CIRI中miR-124/NF-κB/Fas信号通路减轻神经元凋亡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroreport 医学-神经科学

CiteScore

3.20

自引率

0.00%

发文量

150

审稿时长

1 months

期刊介绍： NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.