电针足三里通过抑制背根神经节交感-感觉耦合和神经源性炎症减轻结肠炎大鼠躯体疼痛。

IF 3 4区 医学 Q2 NEUROSCIENCES
Yi-Li Wang, Hai-Yan Zhu, Xi-Qian Lv, Xing-Ying Ren, Ying-Chun Peng, Jin-Yu Qu, Xue-Fang Shen, Ran Sun, Meng-Lu Xiao, Hong Zhang, Zhao-Hui Chen, Peng Cong
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引用次数: 5

摘要

痛觉过敏引发的牵涉性躯体疼痛在炎症性肠病(IBD)患者中很常见。据报道,交感神经纤维进入背根神经节(DGR)的萌芽和神经源性炎症与神经性疼痛、神经元的兴奋性和传入神经有关。本研究旨在探讨电针足三里(ST36)对结肠炎症和痛觉过敏的干预作用及其机制。Sprague-Dawley (SD)随机分为对照、模型、EA和假EA 4组。我们的研究结果显示,EA治疗显著减轻了葡聚糖硫酸钠(DSS-)诱导的结直肠病变和炎症细胞因子的分泌,如TNF-α、IL-1β、PGE2和IL-6。EA对结肠炎大鼠的机械和热痛超敏反应也有抑制作用。重要的是,EA有效地消除了DSS对同侧腰6 (L6) DRG交感-感觉偶联的促进作用,表现为酪氨酸羟化酶- (TH-)阳性交感神经纤维向感觉神经元的芽化和降钙素基因相关肽(CGRP)的共定位。此外,足三里(ST36)的EA激活了神经源性炎症,其特征是L6 DRG对应的结肠炎大鼠皮肤组织中P物质(SP)、透明质酸(HA)、缓激肽(BK)和前列腺素(PGI2)的表达降低。机械上,EA治疗降低了结肠炎大鼠L6 DRG中TRPV1/CGRP、ERK和TLR4信号通路的激活。综上所述,我们推测EA治疗改善了结肠炎症和痛觉过敏,可能是通过使TRPV1/CGRP、ERK和TLR4信号通路失活来抑制交感神经纤维进入L6 DGR和神经源性炎症的生长。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Electroacupuncture Zusanli (ST36) Relieves Somatic Pain in Colitis Rats by Inhibiting Dorsal Root Ganglion Sympathetic-Sensory Coupling and Neurogenic Inflammation.

Electroacupuncture Zusanli (ST36) Relieves Somatic Pain in Colitis Rats by Inhibiting Dorsal Root Ganglion Sympathetic-Sensory Coupling and Neurogenic Inflammation.

Electroacupuncture Zusanli (ST36) Relieves Somatic Pain in Colitis Rats by Inhibiting Dorsal Root Ganglion Sympathetic-Sensory Coupling and Neurogenic Inflammation.

Electroacupuncture Zusanli (ST36) Relieves Somatic Pain in Colitis Rats by Inhibiting Dorsal Root Ganglion Sympathetic-Sensory Coupling and Neurogenic Inflammation.

Referred somatic pain triggered by hyperalgesia is common in patients with inflammatory bowel disease (IBD). It was reported that sprouting of sympathetic nerve fibers into the dorsal root ganglion (DGR) and neurogenic inflammation were related to neuropathic pain, the excitability of neurons, and afferents. The purpose of the study was to explore the potential and mechanism of electroacupuncture (EA) at Zusanli (ST36) for the intervention of colon inflammation and hyperalgesia. Sprague-Dawley (SD) was randomly divided into four groups, including control, model, EA, and sham-EA. Our results showed EA treatment significantly attenuated dextran sulfate sodium- (DSS-) induced colorectal lesions and inflammatory cytokine secretion, such as TNF-α, IL-1β, PGE2, and IL-6. EA also inhibited mechanical and thermal pain hypersensitivities of colitis rats. Importantly, EA effectively abrogated the promotion effect of DSS on ipsilateral lumbar 6 (L6) DRG sympathetic-sensory coupling, manifested as the sprouting of tyrosine hydroxylase- (TH-) positive sympathetic fibers into sensory neurons and colocalization of and calcitonin gene-related peptide (CGRP). Furthermore, EA at Zusanli (ST36) activated neurogenic inflammation, characterized by decreased expression of substance P (SP), hyaluronic acid (HA), bradykinin (BK), and prostacyclin (PGI2) in colitis rat skin tissues corresponding to the L6 DRG. Mechanically, EA treatment reduced the activation of the TRPV1/CGRP, ERK, and TLR4 signaling pathways in L6 DRG of colitis rats. Taken together, we presumed that EA treatment improved colon inflammation and hyperalgesia, potentially by suppressing the sprouting of sympathetic nerve fibers into the L6 DGR and neurogenic inflammation via deactivating the TRPV1/CGRP, ERK, and TLR4 signaling pathways.

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来源期刊
Neural Plasticity
Neural Plasticity NEUROSCIENCES-
CiteScore
6.80
自引率
0.00%
发文量
77
审稿时长
16 weeks
期刊介绍: Neural Plasticity is an international, interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology. Neural Plasticity publishes research and review articles from the entire range of relevant disciplines, including basic neuroscience, behavioral neuroscience, cognitive neuroscience, biological psychology, and biological psychiatry.
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