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肝性脑病氧化应激研究概述:从细胞和基于氨的动物模型到人体数据。

Overview of oxidative stress findings in hepatic encephalopathy: From cellular and ammonium-based animal models to human data.

机构信息

CIBM Center for Biomedical Imaging, Switzerland; Animal Imaging and Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland; Laboratory of Functional and Metabolic Imaging, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.

CIBM Center for Biomedical Imaging, Switzerland; Animal Imaging and Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.

出版信息

Anal Biochem. 2022 Oct 1;654:114795. doi: 10.1016/j.ab.2022.114795. Epub 2022 Jun 24.

DOI:10.1016/j.ab.2022.114795
PMID:35753389
Abstract

Oxidative stress is a natural phenomenon in the body. Under physiological conditions intracellular reactive oxygen species (ROS) are normal components of signal transduction cascades, and their levels are maintained by a complex antioxidants systems participating in the in-vivo redox homeostasis. Increased oxidative stress is present in several chronic diseases and interferes with phagocytic and nervous cell functions, causing an up-regulation of cytokines and inflammation. Hepatic encephalopathy (HE) occurs in both acute liver failure (ALF) and chronic liver disease. Increased blood and brain ammonium has been considered as an important factor in pathogenesis of HE and has been associated with inflammation, neurotoxicity, and oxidative stress. The relationship between ROS and the pathophysiology of HE is still poorly understood. Therefore, sensing ROS production for a better understanding of the relationship between oxidative stress and functional outcome in HE pathophysiology is critical for determining the disease mechanisms, as well as to improve the management of patients. This review is emphasizing the important role of oxidative stress in HE development and documents the changes occurring as a consequence of oxidative stress augmentation based on cellular and ammonium-based animal models to human data.

摘要

氧化应激是体内的一种自然现象。在生理条件下,细胞内的活性氧(ROS)是信号转导级联的正常组成部分,其水平由参与体内氧化还原平衡的复杂抗氧化系统维持。几种慢性疾病中存在氧化应激增加,并干扰吞噬细胞和神经细胞的功能,导致细胞因子和炎症的上调。肝性脑病(HE)发生在急性肝衰竭(ALF)和慢性肝病中。血液和大脑中的铵增加被认为是 HE 发病机制中的一个重要因素,并与炎症、神经毒性和氧化应激有关。ROS 与 HE 病理生理学之间的关系尚不清楚。因此,检测 ROS 的产生对于更好地理解氧化应激与 HE 病理生理学中功能结果之间的关系至关重要,这有助于确定疾病机制,并改善患者的管理。这篇综述强调了氧化应激在 HE 发展中的重要作用,并根据细胞和基于铵的动物模型到人类数据记录了氧化应激增加所导致的变化。

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