Protection of the neurovascular unit from calcium-related ischemic injury by linalyl acetate
DC Field | Value | Language |
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dc.contributor.author | Hsieh, Yu Shan | - |
dc.contributor.author | Shin, You Kyoung | - |
dc.contributor.author | Seol, Geun Hee | - |
dc.date.accessioned | 2021-11-23T10:40:31Z | - |
dc.date.available | 2021-11-23T10:40:31Z | - |
dc.date.created | 2021-08-30 | - |
dc.date.issued | 2021-03 | - |
dc.identifier.issn | 0304-4920 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/128464 | - |
dc.description.abstract | Calcium-related ischemic injury (CRII) can damage cells of the neurovascular unit (NVU). Here, we investigate the protective effects of linalyl acetate (LA) against CRII-induced NVU damage and evaluate the underlying mechanisms. The protective effects of LA in cell lines representative of NVU components (BEND, SH-SY5Y, BV2, and U373 cells) were evaluated following exposure to oxygen-glucose deprivation/reoxygenation alone (OGD/R-only) or OGD/R in the presence of 5 mM extracellular calcium ([Ca2+]o) to mimic CRII. LA reversed damage under OGD/R-only conditions by blocking p47phox/NADPH oxidase (NOX) 2 expression, reactive oxygen species (ROS) production, nitric oxide (NO) abnormality, and lactate dehydrogenase (LDH) release only in the BEND cells. However, under CRII-mimicking conditions, LA reversed NO abnormality and matrix metalloproteinase (MMP)-9 activation in the BEND murine brain endothelial cells; inhibited p47phox expression in the human SH-SY5Y neural-like cells; decreased NOX2 expression and ROS generation in the BV2 murine microglial cells; and reduced p47phox expression in the U373 human astrocyte-like cells. Importantly, LA protected against impairment of the neural cells, astrocytes, and microglia, all of which are cellular components of the NVU induced by exposure to CRII-mimicking conditions, by reducing LDH release. We found that LA exerted a protective effect in the BEND cells that may differ from its protective effects in other NVU cell types, following OGD/R-induced damage in the context of elevated [Ca2+]o. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | WOLTERS KLUWER MEDKNOW PUBLICATIONS | - |
dc.subject | BLOOD-BRAIN-BARRIER | - |
dc.subject | ENDOTHELIAL NITRIC-OXIDE | - |
dc.subject | LACTATE-DEHYDROGENASE | - |
dc.subject | SENSING RECEPTOR | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | STROKE | - |
dc.subject | CELLS | - |
dc.subject | HYPERTENSION | - |
dc.subject | MATRIX-METALLOPROTEINASE-9 | - |
dc.subject | DYSFUNCTION | - |
dc.title | Protection of the neurovascular unit from calcium-related ischemic injury by linalyl acetate | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Seol, Geun Hee | - |
dc.identifier.doi | 10.4103/cjp.cjp_94_20 | - |
dc.identifier.scopusid | 2-s2.0-85105475310 | - |
dc.identifier.wosid | 000646639400004 | - |
dc.identifier.bibliographicCitation | CHINESE JOURNAL OF PHYSIOLOGY, v.64, no.2, pp.88 - 96 | - |
dc.relation.isPartOf | CHINESE JOURNAL OF PHYSIOLOGY | - |
dc.citation.title | CHINESE JOURNAL OF PHYSIOLOGY | - |
dc.citation.volume | 64 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 88 | - |
dc.citation.endPage | 96 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.subject.keywordPlus | BLOOD-BRAIN-BARRIER | - |
dc.subject.keywordPlus | ENDOTHELIAL NITRIC-OXIDE | - |
dc.subject.keywordPlus | LACTATE-DEHYDROGENASE | - |
dc.subject.keywordPlus | SENSING RECEPTOR | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | STROKE | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | HYPERTENSION | - |
dc.subject.keywordPlus | MATRIX-METALLOPROTEINASE-9 | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.subject.keywordAuthor | Calcium-related ischemic injury | - |
dc.subject.keywordAuthor | linalyl acetate | - |
dc.subject.keywordAuthor | neurovascular unit | - |
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