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“废气不废”:气体信号分子硫化氢的研究进展

金红芳, 杜军保, 唐朝枢

北京大学第一医院儿科,北京 100034; 北京大学医学部,北京 100191

摘要

内源性气体信号分子的发现开辟了“废气不废”的新思路。硫化氢(hydrogen sulfide, H2S)是继一氧化氮(nitricoxide, NO)和一氧化碳(carbon monoxide, CO)之后的气体信号分子家系新成员。近年来,人们对H2S 的内源性生成、生物学效应及其机制,特别是其在心血管、神经、呼吸、内分泌等系统的疾病发生、发展过程中的病理生理学意义进行了广泛研究。本文综述了近年来H2S 相关基础、临床以及药学研究方面的进展,包括H2S 对细胞增殖和凋亡、炎症反应、血管新生及离子通道的调节作用,H2S 在各种系统疾病发病中的调节作用,H2S 供体及其在药学领域的研究进展。

关键词: 硫化氢; 增殖; 凋亡; 炎症反应; 血管新生; 离子通道

分类号:R544

[“Waste gas is not waste”: advance in the research of hydrogen sulfide.] [Ariticle in Chinese]

JIN Hong-Fang, DU Jun-Bao, TANG CHAO-SHU

Department of Pediatrics, Peking University First Hospital, Beijing 100034, China; Peking University Health Science Center, Beijing 100191, China

Abstract

The discovery of endogenous gasotransmitters puts forwards a new concept, “waste gas is not waste”. Hydrogen sulfide(H2S) is considered as a new member of gasotransmitter family, following nitric oxide (NO) and carbon monoxide (CO). Recently, theunderstanding of H2S biological effect and its mechanisms has been deepened, especially the pathophysiological significance of H2S inthe various diseases such as cardiovascular diseases, neurological diseases, respiratory diseases, endocrine diseases, etc. This articlereviews recent progress of basic, clinical and pharmacological researches related to endogenous H2S, including the regulatory effects ofH2S on the cell proliferation, apoptosis, inflammation, angiogenesis and ion channels, the role of endogenous H2S pathway in thepathogenesis of various diseases, as well as the study of the H2S donor and H2S-related drugs.

Key words: hydrogen sulfide; proliferation; apoptosis; inflammation; angiogenesis; ion channel

收稿日期:2010-08-29  录用日期:2010-10-09

通讯作者:金红芳  E-mail: jinhongfang51@126.com

引用本文:

金红芳, 杜军保, 唐朝枢. “废气不废”:气体信号分子硫化氢的研究进展[J]. 生理学报 2010; 62 (6): 495-504.

JIN Hong-Fang, DU Jun-Bao, TANG CHAO-SHU. [“Waste gas is not waste”: advance in the research of hydrogen sulfide.] [Ariticle in Chinese] . Acta Physiol Sin 2010; 62 (6): 495-504 (in Chinese with English abstract).