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Effect of Aralia Elata on the Expression of Hyperosmolarity-induced TonEBP Protein and Inflammatory Mediators in Corneal Epithelial Cells

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dc.contributor.authorKim, Seong-Jae-
dc.contributor.authorPark, Mi Hwa-
dc.contributor.authorYoo, Woong-Sun-
dc.contributor.authorHong, Eun-Kyung-
dc.contributor.authorChoi, Mee Young-
dc.contributor.authorChoi, Wan Sung-
dc.date.accessioned2022-12-26T10:45:43Z-
dc.date.available2022-12-26T10:45:43Z-
dc.date.issued2021-02-
dc.identifier.issn0378-6471-
dc.identifier.issn2092-9374-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/4157-
dc.description.abstractPurpose: To investigate the effect of Aralia elata (AE) on hyperosmolar stress-induced tonicity response enhancer-binding protein (TonEBP) expression and changes in the levels of proinflammatory cytokines in immortalized human corneal epithelial cells (hCECs). Methods: Immortalized hCECs were cultured with either 5 or 10 mu g/mL AE for 24 hours, and the medium then changed to a hyperosmotic medium (500 mOsM/L). After hyperosmolar treatment, cell viability and wound-healing assays were performed, and cell proteins subjected to Western blot analysis, immunocytochemistry for TonEBP and NF-kappa B, and tests measuring changes in the levels of oxidative stress markers and inflammatory mediators. Results: AE pretreatment ameliorated hyperosmolarity-induced cell death and the delay in wound-healing in a dose-dependent manner. AE inhibited TonEBP and phospho-NF-kappa B p65 subunit upregulation. AE significantly decreased the expression levels of Bax, 4-HNE, and IL-1 beta; but increased those of Bcl-2, Bcl-xl, and Gpx. Conclusions: AE increased cell viability and wound-healing, and inhibited the hyperosmolar stress-induced upregulation of TonEBP and NF-kappa B. AE may be useful for treatment of patients with certain ocular surface diseases.-
dc.format.extent9-
dc.language한국어-
dc.language.isoKOR-
dc.publisher대한안과학회-
dc.titleEffect of Aralia Elata on the Expression of Hyperosmolarity-induced TonEBP Protein and Inflammatory Mediators in Corneal Epithelial Cells-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.3341/jkos.2021.62.2.164-
dc.identifier.scopusid2-s2.0-85101744090-
dc.identifier.wosid000620709300003-
dc.identifier.bibliographicCitation대한안과학회지, v.62, no.2, pp 164 - 172-
dc.citation.title대한안과학회지-
dc.citation.volume62-
dc.citation.number2-
dc.citation.startPage164-
dc.citation.endPage172-
dc.type.docTypeArticle-
dc.identifier.kciidART002683501-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClassesci-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaOphthalmology-
dc.relation.journalWebOfScienceCategoryOphthalmology-
dc.subject.keywordPlusDRY EYE DISEASE-
dc.subject.keywordPlusKAPPA-B-
dc.subject.keywordPlusPATHOPHYSIOLOGY-
dc.subject.keywordPlusEXTRACT-
dc.subject.keywordPlusDEATH-
dc.subject.keywordAuthorAralia elata-
dc.subject.keywordAuthorCorneal epithelium-
dc.subject.keywordAuthorHypertonic stress Inflammation-
dc.subject.keywordAuthorTonicity response enhancer-binding protein-
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