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分子氢在缺血/再灌注损伤中的保护作用。

The Protective Role of Molecular Hydrogen in Ischemia/Reperfusion Injury.

机构信息

Centre of Experimental Medicine, Slovak Academy of Sciences, Dúbravská cesta 9, 841 04 Bratislava, Slovakia.

出版信息

Int J Mol Sci. 2024 Jul 18;25(14):7884. doi: 10.3390/ijms25147884.

Abstract

Ischemia/reperfusion injury (IRI) represents a significant contributor to morbidity and mortality associated with various clinical conditions, including acute coronary syndrome, stroke, and organ transplantation. During ischemia, a profound hypoxic insult develops, resulting in cellular dysfunction and tissue damage. Paradoxically, reperfusion can exacerbate this injury through the generation of reactive oxygen species and the induction of inflammatory cascades. The extensive clinical sequelae of IRI necessitate the development of therapeutic strategies to mitigate its deleterious effects. This has become a cornerstone of ongoing research efforts in both basic and translational science. This review examines the use of molecular hydrogen for IRI in different organs and explores the underlying mechanisms of its action. Molecular hydrogen is a selective antioxidant with anti-inflammatory, cytoprotective, and signal-modulatory properties. It has been shown to be effective at mitigating IRI in different models, including heart failure, cerebral stroke, transplantation, and surgical interventions. Hydrogen reduces IRI via different mechanisms, like the suppression of oxidative stress and inflammation, the enhancement of ATP production, decreasing calcium overload, regulating cell death, etc. Further research is still needed to integrate the use of molecular hydrogen into clinical practice.

摘要

缺血/再灌注损伤(IRI)是多种临床疾病(包括急性冠状动脉综合征、中风和器官移植)相关发病率和死亡率的重要原因。在缺血期间,会发生严重的缺氧损伤,导致细胞功能障碍和组织损伤。矛盾的是,再灌注会通过产生活性氧和诱导炎症级联反应而加剧这种损伤。IRI 的广泛临床后果需要开发治疗策略来减轻其有害影响。这已成为基础和转化科学研究努力的基石。本文综述了分子氢在不同器官中的 IRI 作用及其作用机制。分子氢是一种选择性抗氧化剂,具有抗炎、细胞保护和信号调节特性。它已被证明在心力衰竭、脑卒中等不同模型中有效减轻 IRI,以及移植和外科干预。氢气通过抑制氧化应激和炎症、增强 ATP 产生、减少钙超载、调节细胞死亡等不同机制来减轻 IRI。仍需要进一步研究将分子氢的使用整合到临床实践中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/760f/11276695/7a720c216073/ijms-25-07884-g001.jpg

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