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dc.contributor.authorKim, Joonki-
dc.contributor.authorFann, David Yang-Wei-
dc.contributor.authorSeet, Raymond Chee Seong-
dc.contributor.authorJo, Dong-Gyu-
dc.contributor.authorMattson, Mark P.-
dc.contributor.authorArumugam, Thiruma V.-
dc.date.accessioned2024-01-20T03:32:33Z-
dc.date.available2024-01-20T03:32:33Z-
dc.date.created2021-09-05-
dc.date.issued2016-09-
dc.identifier.issn1535-1084-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/123736-
dc.description.abstractStroke is the second foremost cause of mortality worldwide and a major cause of long-term disability. Due to changes in lifestyle and an aging population, the incidence of stroke continues to increase and stroke mortality predicted to exceed 12 % by the year 2030. However, the development of pharmacological treatments for stroke has failed to progress much in over 20 years since the introduction of the thrombolytic drug, recombinant tissue plasminogen activator. These alarming circumstances caused many research groups to search for alternative treatments in the form of neuroprotectants. Here, we consider the potential use of phytochemicals in the treatment of stroke. Their historical use in traditional medicine and their excellent safety profile make phytochemicals attractive for the development of therapeutics in human diseases. Emerging findings suggest that some phytochemicals have the ability to target multiple pathophysiological processes involved in stroke including oxidative stress, inflammation and apoptotic cell death. Furthermore, epidemiological studies suggest that the consumption of plant sources rich in phytochemicals may reduce stroke risk, and so reinforce the possibility of developing preventative or neuroprotectant therapies for stroke. In this review, we describe results of preclinical studies that demonstrate beneficial effects of phytochemicals in experimental models relevant to stroke pathogenesis, and we consider their possible mechanisms of action.-
dc.languageEnglish-
dc.publisherHUMANA PRESS INC-
dc.subjectFOCAL CEREBRAL-ISCHEMIA-
dc.subjectNF-KAPPA-B-
dc.subjectINTERCELLULAR-ADHESION MOLECULE-1-
dc.subjectTRANSCRIPTION FACTOR FOXO1-
dc.subjectCELLULAR STRESS RESPONSES-
dc.subjectATTENUATES BRAIN-DAMAGE-
dc.subjectNATURAL-PRODUCTS-
dc.subjectOXIDATIVE STRESS-
dc.subjectISCHEMIA/REPERFUSION INJURY-
dc.subjectNMDA RECEPTOR-
dc.titlePhytochemicals in Ischemic Stroke-
dc.typeArticle-
dc.identifier.doi10.1007/s12017-016-8403-0-
dc.description.journalClass1-
dc.identifier.bibliographicCitationNEUROMOLECULAR MEDICINE, v.18, no.3, pp.283 - 305-
dc.citation.titleNEUROMOLECULAR MEDICINE-
dc.citation.volume18-
dc.citation.number3-
dc.citation.startPage283-
dc.citation.endPage305-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000387851700006-
dc.identifier.scopusid2-s2.0-84969784912-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeReview-
dc.subject.keywordPlusFOCAL CEREBRAL-ISCHEMIA-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusINTERCELLULAR-ADHESION MOLECULE-1-
dc.subject.keywordPlusTRANSCRIPTION FACTOR FOXO1-
dc.subject.keywordPlusCELLULAR STRESS RESPONSES-
dc.subject.keywordPlusATTENUATES BRAIN-DAMAGE-
dc.subject.keywordPlusNATURAL-PRODUCTS-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusISCHEMIA/REPERFUSION INJURY-
dc.subject.keywordPlusNMDA RECEPTOR-
dc.subject.keywordAuthorStroke-
dc.subject.keywordAuthorInflammation-
dc.subject.keywordAuthorNeuronal cell death-
dc.subject.keywordAuthorIschemia-
dc.subject.keywordAuthorNatural products-
dc.subject.keywordAuthorPhytochemical-
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KIST Article > 2016
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