出 处:《Chinese Medical Journal》2011年第21期3576-3582,共7页中华医学杂志(英文版)
基 金:The study was supported by the grants from the Natural Science Foundation of China (No. 81071005 and No. 30770740) and from the Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry (No.[2010]508).
摘 要:Objective This review discusses the current status and progress in studies on the roles of hydrogen sulfide (H2S) in regulation of neurotoxicity, neuroprotection, and neuromodulator, as well as its therapeutic potential for neurodegenerative disorders. Data sources 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". Study selection Articles regarding the regulation of neuronal function, the protection against neuronal damage and neurological diseases, and their possible cellular and molecular mechanisms associated with H2S were selected. Results The inhibited generation of endogenous H2S is implicated in 1-methy-4-phenylpyridinium ion, 6-OHDA, and homocysteine-triggered neurotoxicity. H2S 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. H2S offers anti-oxidant, anti-inflammatory and anti-apoptotic effects, as well as activates ATP-sensitive potassium channels and cystic fibrosis transmembrane conductance regulator CI channels. H2S regulates the long-term potentiation (LTP) and GABAB receptors in the hippocampus, as well as intracellular calcium and pH homeostasis in neurons and gila cells. Conclusions These articles suggest that endogenous H2S may regulate the toxicity of neurotoxin. H2S not only acts as a neuroprotectant but also serves as a novel neuromodulator.Objective This review discusses the current status and progress in studies on the roles of hydrogen sulfide (H2S) in regulation of neurotoxicity, neuroprotection, and neuromodulator, as well as its therapeutic potential for neurodegenerative disorders. Data sources 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". Study selection Articles regarding the regulation of neuronal function, the protection against neuronal damage and neurological diseases, and their possible cellular and molecular mechanisms associated with H2S were selected. Results The inhibited generation of endogenous H2S is implicated in 1-methy-4-phenylpyridinium ion, 6-OHDA, and homocysteine-triggered neurotoxicity. H2S 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. H2S offers anti-oxidant, anti-inflammatory and anti-apoptotic effects, as well as activates ATP-sensitive potassium channels and cystic fibrosis transmembrane conductance regulator CI channels. H2S regulates the long-term potentiation (LTP) and GABAB receptors in the hippocampus, as well as intracellular calcium and pH homeostasis in neurons and gila cells. Conclusions These articles suggest that endogenous H2S may regulate the toxicity of neurotoxin. H2S not only acts as a neuroprotectant but also serves as a novel neuromodulator.
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