Suppr超能文献

应激及早期生活应激在炎症性肠病发病机制中的作用。

Role of stress and early-life stress in the pathogeny of inflammatory bowel disease.

作者信息

Bonaz Bruno, Sinniger Valérie, Pellissier Sonia

机构信息

Université Grenoble Alpes, Service d'Hépato-Gastroentérologie, Grenoble Institut Neurosciences, Grenoble, France.

Université Savoie Mont Blanc, Université Grenoble Alpes, LIP/PC2S, Chambéry, France.

出版信息

Front Neurosci. 2024 Sep 10;18:1458918. doi: 10.3389/fnins.2024.1458918. eCollection 2024.

Abstract

Numerous preclinical and clinical studies have shown that stress is one of the main environmental factor playing a significant role in the pathogeny and life-course of bowel diseases. However, stressful events that occur early in life, even during the fetal life, leave different traces within the central nervous system, in area involved in stress response and autonomic network but also in emotion, cognition and memory regulation. Early-life stress can disrupt the prefrontal-amygdala circuit thus favoring an imbalance of the autonomic nervous system and the hypothalamic-pituitary adrenal axis, resulting in anxiety-like behaviors. The down regulation of vagus nerve and cholinergic anti-inflammatory pathway favors pro-inflammatory conditions. Recent data suggest that emotional abuse at early life are aggravating risk factors in inflammatory bowel disease. This review aims to unravel the mechanisms that explain the consequences of early life events and stress in the pathophysiology of inflammatory bowel disease and their mental co-morbidities. A review of therapeutic potential will also be covered.

摘要

大量临床前和临床研究表明,压力是在肠道疾病的发病机制和病程中起重要作用的主要环境因素之一。然而,早年甚至胎儿期发生的应激事件,会在中枢神经系统内、参与应激反应和自主神经网络的区域以及情绪、认知和记忆调节区域留下不同的痕迹。早年应激会破坏前额叶-杏仁核回路,从而导致自主神经系统和下丘脑-垂体-肾上腺轴失衡,产生焦虑样行为。迷走神经和胆碱能抗炎途径的下调会促进促炎状态。最新数据表明,早年的情感虐待是炎症性肠病的加重危险因素。本综述旨在阐明解释早年事件和应激在炎症性肠病病理生理学及其精神共病中的后果的机制。还将涵盖对治疗潜力的综述。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6716/11420137/5c3cc5be650e/fnins-18-1458918-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验