{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T11:04:41Z","timestamp":1778670281760,"version":"3.51.4"},"reference-count":113,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2016,9,29]],"date-time":"2016-09-29T00:00:00Z","timestamp":1475107200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Although precise cellular and molecular mechanisms underlying neurodegeneration still remain enigmatic, key factors associated with degenerative disorders, such as glutamate toxicity and oxidative stress, have been recently identified. Accordingly, there has been growing interest in examining the effects of exogenous and endogenous molecules on neuroprotection and neurodegeneration. In this paper, we review recent studies on neuroprotective and\/or neurodegenerative effects of natural products, such as caffeic acid and chlorogenic acid, and gaseous mediators, including hydrogen sulfide and nitric oxide. Furthermore, possible molecular mechanisms of these molecules in relation to glutamate signals are discussed. Insight into the pathophysiological role of these molecules will make progress in our understanding of molecular mechanisms underlying neurodegenerative diseases, and is expected to lead to potential therapeutic approaches.<\/jats:p>","DOI":"10.3390\/ijms17101652","type":"journal-article","created":{"date-parts":[[2016,9,29]],"date-time":"2016-09-29T09:54:50Z","timestamp":1475142890000},"page":"1652","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Essential Roles of Natural Products and Gaseous Mediators on Neuronal Cell Death or Survival"],"prefix":"10.3390","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4335-4170","authenticated-orcid":false,"given":"Yoshinori","family":"Mikami","sequence":"first","affiliation":[{"name":"Department of Physiology, School of Medicine, Faculty of Medicine, Toho University, 5-21-16 Omori-Nishi, Ota-ku, Tokyo 143-8540, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sho","family":"Kakizawa","sequence":"additional","affiliation":[{"name":"Department of Biological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Yoshida-Shimoadachi-cho, Sakyo-ku, Kyoto 606-8501, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4368-4794","authenticated-orcid":false,"given":"Toshiko","family":"Yamazawa","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology, The Jikei University School of Medicine, 3-25-8 Nishishimbashi, Minato-ku, Tokyo 105-8461, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2016,9,29]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"353","DOI":"10.1126\/science.1072994","article-title":"The amyloid hypothesis of Alzheimer\u2019s disease: Progress and problems on the road to therapeutics","volume":"297","author":"Hardy","year":"2002","journal-title":"Science"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"964518","DOI":"10.1155\/2015\/964518","article-title":"Mechanisms of neuronal protection against excitotoxicity, endoplasmic reticulum stress, and mitochondrial dysfunction in stroke and neurodegenerative diseases","volume":"2015","author":"Prentice","year":"2015","journal-title":"Oxid. 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