摘要
硫化氢(H2S)作为一种毒性物质,在过去几十年中被公认为一种重要的内源性气体递质,在心血管系统的稳态中发挥着关键作用。近年来,越来越多的证据表明H2S对心肌缺血/再灌注(I/R)具有保护作用,引起了人们对H2S心脏保护作用的可能作用机制的越来越多的兴趣,并发现了多个靶点的参与。目前,通过体内外I/R损伤模型,如抗炎或抗氧化损伤模型,以及Ssuf水化修饰蛋白质如离子通道的机制,已经提出并验证了许多机制。特别关注的是线粒体的保存和抗凋亡机制,最后甚至描述了促进血管生成的作用。同时,能够释放H2S(单独作为H2S供体)或与杂化分子中的另一种药物结合的分子的设计、开发和药理特性,导致了在心脏保护药物的全景中产生新的化学实体。
关键词: 硫化氢,缺血再灌注,心脏保护,H2S供体,气体递质,心肌损伤。
Current Medicinal Chemistry
Title:The Role of Hydrogen Sulfide and H2S-donors in Myocardial Protection Against Ischemia/Reperfusion Injury
Volume: 25 Issue: 34
关键词: 硫化氢,缺血再灌注,心脏保护,H2S供体,气体递质,心肌损伤。
摘要: Hydrogen sulfide (H2S), previously known only as a toxic agent, in the last decades has been recognized as an important endogenous gasotransmitter, playing a key role in the homeostasis of the cardiovascular system. In the last years, the growing evidence about a protective role exhibited by H2S against myocardial ischemia/reperfusion (I/R), led to an increasing interest for the possible mechanism of action accounting for the H2S cardioprotective effect, and to the discovery of the involvement of several targets. Currently, many mechanisms of action have been proposed and verified through in vitro and in vivo models of I/R injury, such as the anti-inflammatory or the anti-oxidant ones, or mechanisms of Ssufhydration able to modify proteins such as ion channels. Particular attention was focused on the mitochondrial preservation and on anti-apoptotic mechanisms, and finally even a pro-angiogenesis effect has been described. At the same time, the design, the development and the pharmacological characterization of moieties able to release H2S, employed alone as H2S-donor, or conjugated with another drug in hybrid molecules, led to the production of novel chemical entities in the panorama of cardioprotective drugs.
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The Role of Hydrogen Sulfide and H2S-donors in Myocardial Protection Against Ischemia/Reperfusion Injury, Current Medicinal Chemistry 2018; 25 (34) . https://dx.doi.org/10.2174/0929867325666180212120504
DOI https://dx.doi.org/10.2174/0929867325666180212120504 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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