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Drug Delivery Systems for the Treatment of Ischemic Stroke

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dc.contributor.authorRhim, Taiyoun-
dc.contributor.authorLee, Dong Yun-
dc.contributor.authorLee, Minhyung-
dc.date.accessioned2022-07-16T07:56:29Z-
dc.date.available2022-07-16T07:56:29Z-
dc.date.created2021-05-12-
dc.date.issued2013-10-
dc.identifier.issn0724-8741-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/161797-
dc.description.abstractStroke is the third leading cause of death in the United States. Reduced cerebral blood flow causes acute damage to the brain due to excitotoxicity, reactive oxygen species (ROS), and ischemia. Currently, the main treatment for stroke is to revive the blood flow by using thrombolytic agents. Reviving blood flow also causes ischemia-reperfusion (I/R) damage. I/R damage results from inflammation and apoptosis and can persist for days to weeks, increasing the infarct size. Drugs can be applied to stroke to intervene in the sub-acute and chronic phases. Chemical, peptide, and genetic therapies have been evaluated to reduce delayed damage to the brain. These drugs have different characteristics, requiring that delivery carriers be developed based on these characteristics. The delivery route is another important factor affecting the efficiency of drug delivery. Various delivery routes have been developed, such as intravenous injection, intranasal administration, and local direct injection to overcome the blood-brain-barrier (BBB). In this review, the delivery carriers and delivery routes for peptide and gene therapies are discussed and examples are provided. Combined with new drugs, drug delivery systems will eventually provide useful treatments for ischemic stroke.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER/PLENUM PUBLISHERS-
dc.titleDrug Delivery Systems for the Treatment of Ischemic Stroke-
dc.typeArticle-
dc.contributor.affiliatedAuthorRhim, Taiyoun-
dc.contributor.affiliatedAuthorLee, Dong Yun-
dc.contributor.affiliatedAuthorLee, Minhyung-
dc.identifier.doi10.1007/s11095-012-0959-2-
dc.identifier.scopusid2-s2.0-84883872986-
dc.identifier.wosid000324074800002-
dc.identifier.bibliographicCitationPHARMACEUTICAL RESEARCH, v.30, no.10, pp.2429 - 2444-
dc.relation.isPartOfPHARMACEUTICAL RESEARCH-
dc.citation.titlePHARMACEUTICAL RESEARCH-
dc.citation.volume30-
dc.citation.number10-
dc.citation.startPage2429-
dc.citation.endPage2444-
dc.type.rimsART-
dc.type.docTypeReview-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaChemistry-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryChemistry, Multidisciplinary-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.subject.keywordPlusBLOOD-BRAIN-BARRIER-
dc.subject.keywordPlusFOCAL CEREBRAL-ISCHEMIA-
dc.subject.keywordPlusRECOMBINANT ADENOASSOCIATED VIRUS-
dc.subject.keywordPlusVEGF GENE DELIVERY-
dc.subject.keywordPlusHEME OXYGENASE-1 PREVENTS-
dc.subject.keywordPlusMESENCHYMAL STEM-CELLS-
dc.subject.keywordPlusCENTRAL-NERVOUS-SYSTEM-
dc.subject.keywordPlusREDUCES INFARCT SIZE-
dc.subject.keywordPlusLOW-MOLECULAR-WEIGHT-
dc.subject.keywordPlus1ST 24 HOURS-
dc.subject.keywordAuthorbrain-
dc.subject.keywordAuthordrug delivery-
dc.subject.keywordAuthorgene delivery-
dc.subject.keywordAuthorischemia-
dc.subject.keywordAuthorstroke-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs11095-012-0959-2-
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