Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway

IF 3.8 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Neurochemical Research Pub Date : 2025-09-11 DOI:10.1007/s11064-025-04547-z

Guihua Tian, Meiyue Wang, Ke He, Xinyi Li, Yang Wu, Huifeng Hao, Fan Zhang, Youxiang Su, Junyi Long, Yi Lin, Zhihao Shang, Liangqing Huang

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引用次数: 0

Abstract

Electroacupuncture (EA) therapy has been shown to significantly alleviate central poststroke pain (CPSP). However, current research on the mechanisms by which EA relieves CPSP is insufficient. This study explored the role of EA in ameliorating central nervous system inflammation in CPSP rats.The CPSP rat model was established by injecting collagenase IV into the right ventral posterolateral nucleus of the thalamus (VPL). The treatment group was treated with 15 Hz and 2 mA continuous wave EA every other day for a total of 8 sessions. The lncRNA MEG3 (MEG3) was knocked down or overexpressed by adeno-associated virus delivery in vivo in the rat brain. Pain thresholds were measured to assess the hypersensitivity of the rats to pain. Immunofluorescence, Nissl staining and enzyme-linked immunosorbent assay (ELISA) were used to assess the levels of MEG3 and glial fibrillary acidic protein (GFAP) in VPL brain tissue, neuronal injury, and the levels of substance P (SP), TNF-α, IL-1β and IL-6 in VPL brain tissue and serum, respectively. The levels of MEG3, Wnt3a, β-catenin and GFAP in VPL brain tissue were assessed by qRT‒PCR or Western blotting. EA inhibits the expression of MEG3 and neuroinflammatory injury in the VPL brain tissue of CPSP rats, ameliorating hyperalgesia symptoms in CPSP rats. The overexpression of MEG3 weakened the inhibitory effect of EA on the Wnt/β-catenin pathway in the VPL region of the brain, exacerbating pain hypersensitivity and neuroinflammatory damage in the brain hemorrhage regions of CPSP rats. Suppressing the expression of MEG3 in the VPL brain tissue of CPSP rats produced a therapeutic effect similar to that of EA intervention. EA could alleviate neuroinflammation and reduce pain in CPSP rats by suppressing the expression of MEG3. EA could regulate the Wnt/β-catenin signaling pathway via MEG3.

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电针通过抑制LncRNA meg3介导的Wnt/β-Catenin信号通路改善CPSP大鼠神经炎症损伤

电针（EA）治疗已被证明可以显著减轻中枢性脑卒中后疼痛（CPSP）。然而，目前对EA缓解CPSP的机制研究不足。本研究探讨EA对CPSP大鼠中枢神经系统炎症的改善作用。通过向丘脑右腹侧后外侧核（VPL）注射胶原酶IV建立CPSP大鼠模型。治疗组采用15 Hz、2 mA连续波EA治疗，每隔一天进行一次，共8次。lncRNA MEG3 （MEG3）在大鼠脑内通过腺相关病毒的体内传递被敲低或过表达。测量疼痛阈值以评估大鼠对疼痛的超敏反应。采用免疫荧光法、尼氏染色法和酶联免疫吸附法（ELISA）检测VPL脑组织、神经元损伤组织中MEG3和胶质原纤维酸性蛋白（GFAP）水平，以及VPL脑组织和血清中P物质（SP）、TNF-α、IL-1β和IL-6水平。采用qRT-PCR或Western blotting检测VPL脑组织中MEG3、Wnt3a、β-catenin、GFAP水平。EA可抑制CPSP大鼠VPL脑组织MEG3表达及神经炎症损伤，改善CPSP大鼠痛觉过敏症状。MEG3过表达减弱了EA对脑VPL区Wnt/β-catenin通路的抑制作用，加重了CPSP大鼠脑出血区疼痛超敏反应和神经炎症损伤。抑制CPSP大鼠VPL脑组织中MEG3的表达可产生与EA干预相似的治疗效果。EA可通过抑制MEG3的表达，减轻CPSP大鼠的神经炎症和疼痛。EA可通过MEG3调控Wnt/β-catenin信号通路。

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来源期刊

Neurochemical Research 医学-神经科学

CiteScore

7.70

自引率

2.30%

发文量

320

审稿时长

6 months

期刊介绍： Neurochemical Research is devoted to the rapid publication of studies that use neurochemical methodology in research on nervous system structure and function. The journal publishes original reports of experimental and clinical research results, perceptive reviews of significant problem areas in the neurosciences, brief comments of a methodological or interpretive nature, and research summaries conducted by leading scientists whose works are not readily available in English.