药学翻译-硫化氢与细胞信号通路

1、药学翻译-硫化氢与细胞信号通路泛瑞翻译作者：Li L, Rose P, Moore PK.Annu Rev Pharmacol Toxicol. 2011; 51:169-87.PMID: 21210746摘要硫化氢（H2S）是胱硫醚-裂解酶（CSE）与其他自发酶类分解半胱氨酸所得的一种气体递质。H2S供体药理学试验与CSE基因敲除小鼠遗传实验表明该血管扩张性气体在血管直径、局部缺血/再灌注损伤心脏应变与炎症调节方面有重要作用。几十年前，已确认H2S可抑制细胞色素c氧化酶，并可降低细胞内能量产生。但近年来，发现该气体存在大量其他的药理学靶标。H2S可激活KATP与瞬时受体电位（TRP）通道，常

2、抑制大电导钙激活钾(BKCa)通道、T型钙通道与M型钙通道。H2S可抑制或激活NF-B核转运，并影响大量激酶的活性，如p38丝裂原活化蛋白激酶（p38 MAPK）、细胞外信号调节激酶（ERK）与Akt等。这些不同效应可能继发于H2S已知的还原性和/或促进细胞内蛋白质半胱氨酸氢硫化的性质。原文：Title: Hydrogen Sulfide and Cell SignalingAuthor: Li L, Rose P, Moore PK.Annu Rev Pharmacol Toxicol. 2011; 51:169-87.PMID: 21210746AbstractHydrogen sulfi

3、de (H2S) is a gaseous mediator synthesized from cysteine by cystathionine lyase (CSE) and other naturally occurring enzymes. Pharmacological experiments using H2S donors and genetic experiments using CSE knockout mice suggest important roles for this vasodilator gas in the regulation of blood vessel

4、 caliber, cardiac response to ischemia/reperfusion injury, and inflammation. That H2S inhibits cytochrome c oxidase and reduces cell energy production has been known for many decades, but more recently, a number of additional pharmacological targets for this gas have been identified. H2S activates K

5、ATP and transient receptor potential (TRP) channels but usually inhibits big conductance Ca2+-sensitive K+ (BKCa) channels, T-type calcium channels, and M-type calcium channels. H2S may inhibit or activate NF-B nuclear translocation while affecting the activity of numerous kinases including p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt. These disparate effects may be secondary to the well-known reducing activity of H2S and/or its ability to promote sul