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迷走神经刺激对炎症性肠病的治疗潜力

Therapeutic Potential of Vagus Nerve Stimulation for Inflammatory Bowel Diseases.

作者信息

Bonaz Bruno, Sinniger Valérie, Pellissier Sonia

机构信息

Division of Hepato-Gastroenterology, Centre Hospitalier Universitaire Grenoble Alpes, Grenoble, France.

Grenoble Institute of Neurosciences, Inserm U1216, University Grenoble Alpes, Grenoble, France.

出版信息

Front Neurosci. 2021 Mar 22;15:650971. doi: 10.3389/fnins.2021.650971. eCollection 2021.

Abstract

The vagus nerve is a mixed nerve, comprising 80% afferent fibers and 20% efferent fibers. It allows a bidirectional communication between the central nervous system and the digestive tract. It has a dual anti-inflammatory properties via activation of the hypothalamic pituitary adrenal axis, by its afferents, but also through a vago-vagal inflammatory reflex involving an afferent (vagal) and an efferent (vagal) arm, called the cholinergic anti-inflammatory pathway. Indeed, the release of acetylcholine at the end of its efferent fibers is able to inhibit the release of tumor necrosis factor (TNF) alpha by macrophages via an interneuron of the enteric nervous system synapsing between the efferent vagal endings and the macrophages and releasing acetylcholine. The vagus nerve also synapses with the splenic sympathetic nerve to inhibit the release of TNF-alpha by splenic macrophages. It can also activate the spinal sympathetic system after central integration of its afferents. This anti-TNF-alpha effect of the vagus nerve can be used in the treatment of chronic inflammatory bowel diseases, represented by Crohn's disease and ulcerative colitis where this cytokine plays a key role. Bioelectronic medicine, via vagus nerve stimulation, may have an interest in this non-drug therapeutic approach as an alternative to conventional anti-TNF-alpha drugs, which are not devoid of side effects feared by patients.

摘要

迷走神经是一种混合神经,由80%的传入纤维和20%的传出纤维组成。它允许中枢神经系统与消化道之间进行双向通信。它具有双重抗炎特性,通过其传入纤维激活下丘脑-垂体-肾上腺轴,也通过一种迷走-迷走神经炎性反射,该反射涉及一条传入(迷走)臂和一条传出(迷走)臂,称为胆碱能抗炎途径。实际上,其传出纤维末端乙酰胆碱的释放能够通过肠神经系统的中间神经元抑制巨噬细胞释放肿瘤坏死因子(TNF)α,该中间神经元在传出迷走神经末梢与巨噬细胞之间形成突触并释放乙酰胆碱。迷走神经还与脾交感神经形成突触,以抑制脾巨噬细胞释放TNF-α。在其传入纤维进行中枢整合后,它还可以激活脊髓交感神经系统。迷走神经的这种抗TNF-α作用可用于治疗以克罗恩病和溃疡性结肠炎为代表的慢性炎症性肠病,在这些疾病中这种细胞因子起着关键作用。生物电子医学通过迷走神经刺激,可能会对这种非药物治疗方法感兴趣,将其作为传统抗TNF-α药物的替代方案,而传统药物并非没有患者所担心的副作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bab3/8019822/601ecc3395ae/fnins-15-650971-g001.jpg

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