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电针在中枢水平治疗神经性疼痛的镇痛机制:基于动物实验的研究综述

The analgesic mechanism of electroacupuncture at the central level for neuropathic pain: a review of studies based on animal experiments.

作者信息

Qi Pengfei, Li Quan, Han Mingyuan, Cui Yang, Zhou Xinyu, Sun Zhongren, Ding Shuo, Yu Mengdi, Zhang Hongbo, Yin Hongna

机构信息

Heilongjiang University of Chinese Medicine, Harbin, China.

The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China.

出版信息

Front Neurol. 2025 May 29;16:1587471. doi: 10.3389/fneur.2025.1587471. eCollection 2025.

Abstract

This article analyzes the progress of animal experiments on the analgesic mechanism of electroacupuncture (EA) at the central level for neuropathic pain (NP) in the past 10 years, and summarizes the analgesic mechanism of EA at the central level for NP. EA, as a safe and reliable treatment, can treat NP by regulating the release of nociceptive neurotransmitters and receptors, upregulating the expression of non-coding RNA (ncRNA), inhibiting the activation of microglia, Ca/calmodulin kinase II (CaMKII) phosphorylation, dendritic spine remodeling, endoplasmic reticulum stress (ERS), and glucose metabolism. NP is a type of pain caused by various diseases. Pain caused by stroke, spinal cord injury, postherpetic neuralgia (PHN), diabetes, and chemotherapy-induced neuropathy all fall into the category of NP, which makes the treatment of NP very challenging. At present, EA research on the treatment of NP is more focused on the mechanism of the dorsal horn of the spinal cord, and there are relatively few animal experiments at the level of the central brain region. There is also a lack of clinical trials using human subjects and relevant biochemical indicators. In the future, electrophysiology, neuron tracing, and multi-omics techniques combined with emerging technologies such as artificial intelligence should be used to further improve the analgesic mechanism of EA on the central level for NP, making EA the best treatment for NP.

摘要

本文分析了过去10年动物实验在电针(EA)治疗中枢性神经病理性疼痛(NP)镇痛机制方面的进展,并总结了EA治疗中枢性NP的镇痛机制。EA作为一种安全可靠的治疗方法,可通过调节伤害性神经递质和受体的释放、上调非编码RNA(ncRNA)的表达、抑制小胶质细胞的激活、钙/钙调蛋白激酶II(CaMKII)磷酸化、树突棘重塑、内质网应激(ERS)和葡萄糖代谢来治疗NP。NP是由各种疾病引起的一种疼痛。中风、脊髓损伤、带状疱疹后神经痛(PHN)、糖尿病和化疗引起的神经病变所导致的疼痛都属于NP范畴,这使得NP的治疗极具挑战性。目前,EA治疗NP的研究更多集中在脊髓背角机制,而在中枢脑区水平的动物实验相对较少。同时也缺乏以人体为对象的临床试验及相关生化指标。未来,应采用电生理学、神经元示踪和多组学技术,并结合人工智能等新兴技术,进一步完善EA治疗中枢性NP的镇痛机制,使EA成为治疗NP的最佳方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7d/12158743/f51f74a7c203/fneur-16-1587471-g001.jpg

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