Electroacupuncture inhibits the expression of HMGB1/RAGE and alleviates injury to the primary motor cortex in rats with cerebral ischemia.

IF 1.8 4区 医学 Q4 NEUROSCIENCES Translational Neuroscience Pub Date : 2023-10-09 eCollection Date: 2023-01-01 DOI:10.1515/tnsci-2022-0316
Zeyin Nie, Huachun Miao, Chenyu Li, Feng Wu
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Abstract

Background: The high-mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) signaling pathway holds promise as a potential therapeutic target for ischemic brain injury. The effects of FPS-ZM1 and electroacupuncture (EA) on activation of the HMGB1/RAGE signaling pathway after cerebral ischemia remain uncertain.

Methods: Middle cerebral artery occlusion (MCAO) model was established. Neurological function was assessed using Longa scores. Nissl staining was used to observe the morphology of neurons. The expression levels of HMGB1 and RAGE were assayed with immunofluorescence staining and western blot.

Results: The results showed that EA and FPS-ZM1 could reduce the neural function score and neurons cell injury in cerebral ischemia rats by inhibiting the expression of HMGB1 and RAGE in primary motor cortex (M1) region. In addition, EA combined with FPS-ZM1 had a better therapeutic effect.

Conclusions: The HMGB1/RAGE pathway could be activated after cerebral ischemia. Both EA and FPS-ZM1 improved neurological deficits and attenuated neuronal damage in rats. They had synergistic effects. These interventions were observed to mitigate brain damage by suppressing the activation of HMGB1/RAGE.

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电针抑制脑缺血大鼠HMGB1/RAGE的表达并减轻对初级运动皮层的损伤。
背景:高迁移率族盒1(HMGB1)/晚期糖基化终产物受体(RAGE)信号通路有望成为缺血性脑损伤的潜在治疗靶点。FPS-ZM1和电针对脑缺血后HMGB1/RAGE信号通路激活的影响尚不确定。方法:建立大脑中动脉闭塞(MCAO)模型。使用Longa评分评估神经功能。采用尼氏染色法观察神经元形态。免疫荧光染色和蛋白质印迹法检测HMGB1和RAGE的表达水平。结果:电针和FPS-ZM1可通过抑制初级运动皮层(M1)HMGB1和RAGE的表达,降低脑缺血大鼠的神经功能评分和神经元细胞损伤。电针配合FPS-ZM1治疗效果较好。结论:脑缺血后可激活HMGB1/RAGE通路。电针和FPS-ZM1均能改善大鼠的神经功能缺损,减轻神经元损伤。它们具有协同效应。观察到这些干预措施通过抑制HMGB1/RAGE的激活来减轻脑损伤。
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来源期刊
CiteScore
3.00
自引率
4.80%
发文量
45
审稿时长
>12 weeks
期刊介绍: Translational Neuroscience provides a closer interaction between basic and clinical neuroscientists to expand understanding of brain structure, function and disease, and translate this knowledge into clinical applications and novel therapies of nervous system disorders.
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