DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hou, Jingang | ko |
dc.contributor.author | Cui, Changhao | ko |
dc.contributor.author | Kim, Sun Chang | ko |
dc.contributor.author | Sung, Changkeun | ko |
dc.contributor.author | Choi, Chulhee | ko |
dc.date.accessioned | 2018-03-23T00:14:32Z | - |
dc.date.available | 2018-03-23T00:14:32Z | - |
dc.date.created | 2018-03-20 | - |
dc.date.created | 2018-03-20 | - |
dc.date.issued | 2018-03 | - |
dc.identifier.citation | CHEMICO-BIOLOGICAL INTERACTIONS, v.283, pp.75 - 83 | - |
dc.identifier.issn | 0009-2797 | - |
dc.identifier.uri | http://hdl.handle.net/10203/240923 | - |
dc.description.abstract | Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by D-galactose via suppressing p38MAPK-dependent NF-kappa B activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-kappa B inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-kappa B was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases. | - |
dc.language | English | - |
dc.publisher | ELSEVIER IRELAND LTD | - |
dc.subject | DNA-DAMAGE RESPONSE | - |
dc.subject | INFLAMMATORY CYTOKINE SECRETION | - |
dc.subject | AGING-RELATED DISEASE | - |
dc.subject | CELLULAR SENESCENCE | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | KAPPA-B | - |
dc.subject | EXPRESSION | - |
dc.subject | BRAIN | - |
dc.subject | MICE | - |
dc.subject | PROLIFERATION | - |
dc.title | Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype | - |
dc.type | Article | - |
dc.identifier.wosid | 000425896600009 | - |
dc.identifier.scopusid | 2-s2.0-85041417644 | - |
dc.type.rims | ART | - |
dc.citation.volume | 283 | - |
dc.citation.beginningpage | 75 | - |
dc.citation.endingpage | 83 | - |
dc.citation.publicationname | CHEMICO-BIOLOGICAL INTERACTIONS | - |
dc.identifier.doi | 10.1016/j.cbi.2018.02.002 | - |
dc.contributor.localauthor | Kim, Sun Chang | - |
dc.contributor.localauthor | Choi, Chulhee | - |
dc.contributor.nonIdAuthor | Hou, Jingang | - |
dc.contributor.nonIdAuthor | Cui, Changhao | - |
dc.contributor.nonIdAuthor | Sung, Changkeun | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | Astrocytic senescent | - |
dc.subject.keywordAuthor | Ginsenoside F1 | - |
dc.subject.keywordAuthor | p38MAPK | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | SASP | - |
dc.subject.keywordAuthor | Glioblastoma | - |
dc.subject.keywordPlus | DNA-DAMAGE RESPONSE | - |
dc.subject.keywordPlus | INFLAMMATORY CYTOKINE SECRETION | - |
dc.subject.keywordPlus | AGING-RELATED DISEASE | - |
dc.subject.keywordPlus | CELLULAR SENESCENCE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | KAPPA-B | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | BRAIN | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | PROLIFERATION | - |
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