Glycyrrhizin inhibits human neutrophil elastase-induced mucin 5AC overproduction in human bronchial epithelial cells / 中南大学学报(医学版)
Journal of Central South University(Medical Sciences)
;
(12): 252-257, 2014.
Artículo
en Chino
| WPRIM
| ID: wpr-815431
ABSTRACT
OBJECTIVE@#To investigate the effect of glycyrrhizin (Gly) on human neutrophil elastase (HNE)- induced mucin (MUC) 5AC overproduction in human bronchial epithelial cells (16HBE), and the potential signaling pathway involved in this process.@*METHODS@#The cultured cells were divided into 3 groups a control group, cultured in serum-free DMEM medium; an HNE group, pretreated with HNE alone; and a Gly group, incubated with HNE and Gly. After stimulation with a variety of Gly concentrations, the cytotoxicity was assessed by methyl thiazolyl tetrazolium method. The mRNA expressions of p38, nuclear factor κB (NF-κB) p65, inhibitory κBα (IκBα) and MUC5AC were detected by real-time PCR. The phosphorylation levels of p38 (p-p38), NF-κB p65 (p-NF-κB p65) and IκBα (p-IκBα) were measured by Western blot while the levels of MUC5AC protein were analyzed by emzyme-linked immunosorbent assay and immunofluorescence.@*RESULTS@#Compared with the control group, the expression levels of MUC5AC mRNA and protein in the HNE group were both significantly increased. There was a significant increase in p-p38 and p-NF-κB p65, while the production of IκBα was much lower than that in the control group. Gly significantly inhibited the increase of MUC5AC, p38 and NF-κB p65, but increased the activity of IκBα.@*CONCLUSION@#Glycyrrhizin can inhibit MUC5AC overproduction via p38-NF-κB p65/IκBα signaling pathway.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Farmacología
/
Fosforilación
/
Bronquios
/
Transducción de Señal
/
Línea Celular
/
Elastasa de Leucocito
/
Ácido Glicirrínico
/
Proteínas I-kappa B
/
Biología Celular
/
Proteínas Quinasas p38 Activadas por Mitógenos
Límite:
Humanos
Idioma:
Chino
Revista:
Journal of Central South University(Medical Sciences)
Año:
2014
Tipo del documento:
Artículo
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