Department of Physiology, Institute of Cognition and Nervous Systems Disease, Medical College, University of South China, Hengyang, Hunan 421001, China.
Chin Med J (Engl). 2011 Nov;124(21):3576-82.
This review discusses the current status and progress in studies on the roles of hydrogen sulfide (H(2)S) in regulation of neurotoxicity, neuroprotection, and neuromodulator, as well as its therapeutic potential for neurodegenerative disorders.
The data used in this review were mainly from Medline and PubMed published in English from 2001 to August 2011. The search terms were "hydrogen sulfide", "neuron", and "neurodegenerative disorders".
Articles regarding the regulation of neuronal function, the protection against neuronal damage and neurological diseases, and their possible cellular and molecular mechanisms associated with H(2)S were selected.
The inhibited generation of endogenous H(2)S is implicated in 1-methy-4-phenylpyridinium ion, 6-OHDA, and homocysteine-triggered neurotoxicity. H(2)S elicits neuroprotection in Alzheimer's disease and Parkinson's disease models as well as protecting neurons against oxidative stress, ischemia, and hypoxia-induced neuronal death. H(2)S offers anti-oxidant, anti-inflammatory and anti-apoptotic effects, as well as activates ATP-sensitive potassium channels and cystic fibrosis transmembrane conductance regulator Cl- channels. H(2)S regulates the long-term potentiation (LTP) and GABAB receptors in the hippocampus, as well as intracellular calcium and pH homeostasis in neurons and glia cells.
These articles suggest that endogenous H(2)S may regulate the toxicity of neurotoxin. H(2)S not only acts as a neuroprotectant but also serves as a novel neuromodulator.
本综述讨论了硫化氢(H(2)S)在调节神经毒性、神经保护和神经调质中的作用及其在神经退行性疾病中的治疗潜力的现状和进展。
本综述中使用的数据主要来自 2001 年至 2011 年 8 月期间以英文发表在 Medline 和 PubMed 上的文献。检索词为“硫化氢”、“神经元”和“神经退行性疾病”。
选择了与 H(2)S 相关的调节神经元功能、保护神经元免受损伤和神经疾病及其可能的细胞和分子机制的文章。
内源性 H(2)S 的生成抑制与 1-甲基-4-苯基吡啶鎓、6-羟多巴胺和同型半胱氨酸触发的神经毒性有关。H(2)S 在阿尔茨海默病和帕金森病模型中具有神经保护作用,还能保护神经元免受氧化应激、缺血和缺氧诱导的神经元死亡。H(2)S 具有抗氧化、抗炎和抗细胞凋亡作用,并激活 ATP 敏感性钾通道和囊性纤维化跨膜电导调节氯通道。H(2)S 调节海马中的长时程增强(LTP)和 GABAB 受体,以及神经元和神经胶质细胞中的细胞内钙和 pH 稳态。
这些文章表明内源性 H(2)S 可能调节神经毒素的毒性。H(2)S 不仅作为神经保护剂,而且作为新型神经调质。