Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/103760
DC Field | Value | Language |
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dc.contributor.author | Sousa, Cátia | - |
dc.contributor.author | Neves, Bruno Miguel | - |
dc.contributor.author | Leitão, Alcino Jorge | - |
dc.contributor.author | Mendes, Alexandrina Ferreira | - |
dc.date.accessioned | 2022-11-25T09:59:59Z | - |
dc.date.available | 2022-11-25T09:59:59Z | - |
dc.date.issued | 2021-07-04 | - |
dc.identifier.issn | 2227-9059 | pt |
dc.identifier.uri | https://hdl.handle.net/10316/103760 | - |
dc.description.abstract | The signaling pathways involved in age-related inflammation are increasingly recognized as targets for the development of preventive and therapeutic strategies. Our previous study elucidated the structure-activity relationship of monoterpene compounds derived from p-menthane as potential anti-inflammatory drugs and identified (S)-(+)-carvone as the most potent among the compounds tested. This study aims at identifying the molecular mechanism underlying the anti-inflammatory properties of (S)-(+)-carvone. The murine macrophage cell line, Raw 264.7, was stimulated with bacterial lipopolysaccharide (LPS) to simulate inflammation. Western blot was used to assess protein levels and post-translational modifications. The subcellular localization of NF-κB/p65 was visualized by immunocytochemistry. An in vitro fluorometric assay was used to measure Sirtuin-1 (SIRT1) activity. (S)-(+)-carvone inhibited LPS-induced JNK1 phosphorylation, but not that of p38 and ERK1/2 and also did not affect the phosphorylation and degradation of the NF-κB inhibitor, IκB-α. Accordingly, (S)-(+)-carvone did not affect LPS-induced phosphorylation of NF-κB/p65 on Ser536 and its nuclear translocation, but it significantly decreased LPS-induced IκB-α resynthesis, a NF-κB-dependent process, and NF-κB/p65 acetylation on lysine (Lys) 310. Deacetylation of that Lys residue is dependent on the activity of SIRT1, which was found to be increased by (S)-(+)-carvone, while its protein levels were unaffected. Taken together, these results show that (S)-(+)-carvone is a new SIRT1 activator with the potential to counteract the chronic low-grade inflammation characteristic of age-related diseases. | pt |
dc.language.iso | eng | pt |
dc.relation | POCI-01-0145-FEDER-CARTILFACTORY | pt |
dc.relation | CENTRO-01-0145-FEDER-HealthyAging2020 | pt |
dc.relation | POCI-01-0145-FEDER-028424 | pt |
dc.relation | CENTRO-01-0145- FEDER-007440 | pt |
dc.relation | UIDB/04539/2020 | pt |
dc.relation | UIDP/04539/2020 | pt |
dc.relation | PhD fellowship, SFRH/79600/2011 | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt |
dc.subject | aging | pt |
dc.subject | inflammation | pt |
dc.subject | monoterpene | pt |
dc.subject | NF- B | pt |
dc.subject | Sirtuin-1 | pt |
dc.subject | Sirtuin-1 activating compound | pt |
dc.title | Elucidation of the Mechanism Underlying the Anti-Inflammatory Properties of (S)-(+)-Carvone Identifies a Novel Class of Sirtuin-1 Activators in a Murine Macrophage Cell Line | pt |
dc.type | article | - |
degois.publication.firstPage | 777 | pt |
degois.publication.issue | 7 | pt |
degois.publication.title | Biomedicines | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.3390/biomedicines9070777 | pt |
degois.publication.volume | 9 | pt |
dc.date.embargo | 2021-07-04 | * |
uc.date.periodoEmbargo | 0 | pt |
item.grantfulltext | open | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.openairetype | article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | Com Texto completo | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0001-5511-7132 | - |
Appears in Collections: | I&D CNC - Artigos em Revistas Internacionais FFUC- Artigos em Revistas Internacionais I&D CIBB - Artigos em Revistas Internacionais |
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