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Effects of dexamethasone and interleukin-10 on production of pro-inflammatory cytokines and activation of nuclear transcriptional factors in cultured human peripheral blood mononuclear cells / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)2000.
Artículo en Chino | WPRIM | ID: wpr-519975
ABSTRACT

AIM:

To observe the effects of dexamethasone and interleukin-10 (IL-10) on the release of proinflammatory cytokines, tumor necrosis factor-?(TNF-?), IL-6 and activation of transcriptional factors, nuclear factor-?B(NF-?B), activator protein-1 (AP-1) and cAMP response element binding protein (CREB) in cultrued human peripheral blood mononuclear cells (hPBMC).

METHODS:

The hPBMC were divided into control group, lipopolysaccharide (LPS) stimulated group, dexamethasone and IL-10 treated group. The contents of TNF-? and IL-6 in supernatant were mensured by ELISA. The activity of NF-?B, AP-1 and CREB of nuclear abstract were analyzed by electrophoretic morbility shift assay (EMSA).

RESULTS:

The content of TNF-? was significantly increased 1 hour after LPS stimulation, and it was significantly inhibition by dexamethasone and IL-10. The contents of IL-6 and IL-10 were significantly increased after LPS stimulation for 12 hours. The production of IL-6 was still inhibited by dexamethasone and IL-10, but the production of IL-10 was not affected by dexamethasone. The activities of NF-?B, AP-1 and CREB were significantly increased 1 hour after LPS stimulation. Dexamethasone and IL-10 significantly ihibited their activities, but the effects of dexamethasone was stronger than that of IL-10.

CONCLUSIONS:

LPS induces the release of several pro and anti- inflammatory cytokines and induces the activation of several transcriptional factors in hPBMC. Dexamethasone and IL-10 can inhibite the production of proinflammatory cytokines TNF-?, IL-6 and the activation of NF-?B, AP-1 and CREB. Dexamthasone has more significant inhibitory effect on AP-1 and CREB than IL-10.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 2000 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 2000 Tipo del documento: Artículo