Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Más filtros











Base de datos
Intervalo de año de publicación
1.
Pharmazie ; 75(9): 436-439, 2020 09 01.
Artículo en Inglés | MEDLINE | ID: mdl-32797769

RESUMEN

Our study investigated the effects of acacetin, a natural flavonoid compound, on the survival and expression of inflammatory related cytokines in lipopolysaccharide (LPS)-stimulated human periodontal ligament (PDL) cells. Treatment with acacetin significantly promoted survival and suppressed apoptosis in LPS-stimulated PDL cells in a dose-dependent manner, as shown by CCK-8 and flow cytometry assays, respectively. Moreover, ELISA assay showed that acacetin dose-dependently attenuated LPS-induced increases of TNF-α, IL-6 and IL-1ß in PDL cells. Western blot analysis showed that administration of acacetin dose-dependently increased the ratio of LC3II/LC3I, as well as the expression of beclin-1, as compared to LPS-stimulated PDL cells. Inhibition of autophagy by rapamycin, an autophagy inhibitor, increased the production of pro-inflammatory cytokines and decreased survival, abolishing the beneficial role of acacetin in LPS-stimulated PDL cells. In addition, the expression of GSK-3ß, a regulator of autophagy, was suppressed by administration with acacetin in a dose-dependent manner. Acacetin treatment promotes survival and suppresses inflammation in LPS-stimulated PDL cells via regulating autophagy and GSK-3ß signal in PDL cells, suggesting that acacetin may be a potential novel agent for the treatment of chronic periodontitis.


Asunto(s)
Autofagia/efectos de los fármacos , Flavonas/farmacología , Inflamación/tratamiento farmacológico , Ligamento Periodontal/efectos de los fármacos , Antiinflamatorios/administración & dosificación , Antiinflamatorios/farmacología , Apoptosis/efectos de los fármacos , Células Cultivadas , Citocinas/metabolismo , Relación Dosis-Respuesta a Droga , Flavonas/administración & dosificación , Glucógeno Sintasa Quinasa 3 beta/metabolismo , Humanos , Inflamación/patología , Lipopolisacáridos , Ligamento Periodontal/citología
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA