3,4,5-Tricaffeoylquinic Acid Attenuates TRAIL-induced Apoptosis in Human Keratinocytes by Suppressing Apoptosis-related Protein Activation
DC Field | Value | Language |
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dc.contributor.author | Lee, Da Hee | - |
dc.contributor.author | Nam, Yoon Jeong | - |
dc.contributor.author | Lee, Min Sung | - |
dc.contributor.author | Sohn, Dong Suep | - |
dc.contributor.author | Shin, Yong Kyoo | - |
dc.contributor.author | Lee, Chung Soo | - |
dc.date.available | 2019-03-08T16:39:14Z | - |
dc.date.issued | 2015-10 | - |
dc.identifier.issn | 0951-418X | - |
dc.identifier.issn | 1099-1573 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/9041 | - |
dc.description.abstract | Caffeoyl derivatives exhibit antiinflammatory and antioxidant effects. However, the effect of 3,4,5-tricaffeoylquinic acid on the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in keratinocytes that may be involved in skin diseases has not been studied. In this respect, we investigated the effect of 3,4,5-tricaffeoylquinic acid on TRAIL-induced apoptosis in human keratinocytes. 3,4,5-Tricaffeoylquinic acid and oxidant scavengers attenuated the decrease in the cytosolic levels of Bid, Bcl-2, and survivin proteins; the increase in the levels of cytosolic Bax, p53, and phosphorylated p53; the increase in the levels of phosphorylated p38; the increase in the mitochondrial levels of the voltage-dependent anion channel; loss of the mitochondrial transmembrane potential; the release of cytochrome c; activation of caspases (8, 9, and 3); cleavage of poly [ADP-ribose] polymerase-1; production of reactive oxygen species; the depletion of glutathione (GSH); nuclear damage; and cell death in keratinocytes treated with TRAIL. These results suggest that 3,4,5-tricaffeoylquinic acid may reduce TRAIL-induced apoptosis in human keratinocytes by suppressing the activation of the caspase-8 and Bid pathways and the mitochondria-mediated cell death pathway. The effect appears to be associated with the inhibitory effect on the production of reactive oxygen species and depletion of GSH. 3,4,5-Tricaffeoylquinic acid appears to be effective in the prevention of TRAIL-induced apoptosis-mediated skin diseases. Copyright (c) 2015 John Wiley & Sons, Ltd. | - |
dc.format.extent | 10 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY | - |
dc.title | 3,4,5-Tricaffeoylquinic Acid Attenuates TRAIL-induced Apoptosis in Human Keratinocytes by Suppressing Apoptosis-related Protein Activation | - |
dc.type | Article | - |
dc.identifier.doi | 10.1002/ptr.5425 | - |
dc.identifier.bibliographicCitation | PHYTOTHERAPY RESEARCH, v.29, no.10, pp 1549 - 1558 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000362792900012 | - |
dc.identifier.scopusid | 2-s2.0-84943575105 | - |
dc.citation.endPage | 1558 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 1549 | - |
dc.citation.title | PHYTOTHERAPY RESEARCH | - |
dc.citation.volume | 29 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | TRAIL | - |
dc.subject.keywordAuthor | 3, 4, 5-tricaffeoylquinic acid | - |
dc.subject.keywordAuthor | human keratinocytes | - |
dc.subject.keywordAuthor | apoptosis-related protein activation | - |
dc.subject.keywordAuthor | skin diseases | - |
dc.subject.keywordPlus | INDUCED CELL-DEATH | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | ATOPIC-DERMATITIS | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | CANCER-THERAPY | - |
dc.subject.keywordPlus | MITOCHONDRIA | - |
dc.subject.keywordPlus | PATHWAYS | - |
dc.subject.keywordPlus | JNK | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | SKIN | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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