应激性肝损伤机制的文献综述。
A literature review for the mechanisms of stress-induced liver injury.
机构信息
Liver and Immunology Research Center, Daejeon Oriental Hospital of Daejeon University, Daejeon, Korea.
Korean Medicine Convergence Research Division, Korea Institute of Oriental Medicine (KIOM), Daejeon, Korea.
出版信息
Brain Behav. 2019 Mar;9(3):e01235. doi: 10.1002/brb3.1235. Epub 2019 Feb 13.
INTRODUCTION
Experimental studies and clinical observations have shown that stress can damage hepatic tissue both directly and indirectly. Many studies have partially revealed the contributors of stress-induced liver injury; however, the whole process has not yet been uncovered. This review aims to summarize the mechanisms that have been proposed to be involved.
METHODS
A literature search was conducted using PubMed (http://www.ncbi.nlm.nih.gov/pubmed) in its entirety up to March 2018, and analyzed the animal-derived mechanistic studies on stress-induced liver injury.
RESULTS
The liver is the organ that meets and filters a mass of alien material, and then maintains immune tolerance under physiological conditions. Under stress conditions, however, immune tolerance is interrupted, which results in the induction of inflammation in the liver. Contributors to this process can be categorized as follows: hypoxia-reoxygenation, over-activation of Kupffer cells and oxidative stress, influx of gut-derived lipopolysaccharide and norepinephrine, and over-production of stress hormones and activation of the sympathetic nerve.
CONCLUSIONS
Psychological stress is associated with a variety of pathological conditions resulting in liver injury through multiple systems, including the sympathetic nervous and adrenocortical system. Mechanistic understanding of this phenomenon is important for the clinical practice of managing patients with hepatic disorders and should be explored further in the future.
简介
实验研究和临床观察表明,应激可直接和间接损害肝组织。许多研究部分揭示了应激性肝损伤的原因;然而,整个过程尚未被揭示。本综述旨在总结已提出的可能涉及的机制。
方法
通过检索截至 2018 年 3 月的 PubMed(http://www.ncbi.nlm.nih.gov/pubmed)数据库,分析了应激性肝损伤的动物源性机制研究的文献。
结果
肝脏是接触和过滤大量异物的器官,然后在生理条件下维持免疫耐受。然而,在应激条件下,免疫耐受被中断,导致肝脏炎症的诱导。这一过程的促成因素可分为以下几类:缺氧-再氧合、库普弗细胞过度激活和氧化应激、肠道来源的脂多糖和去甲肾上腺素内流、应激激素过度产生和交感神经激活。
结论
心理应激与多种病理状况相关,通过包括交感神经系统和肾上腺皮质系统在内的多个系统导致肝损伤。对这一现象的机制理解对于管理肝障碍患者的临床实践很重要,未来应进一步探索。