Emodin Isolated from Polygoni cuspidati Radix Inhibits TNF-alpha and IL-6 Release by Blockading NF-kappaB and MAP Kinase Pathways in Mast Cells Stimulated with PMA Plus A23187
Biomolecules & Therapeutics
;
: 435-441, 2013.
Artigo
em Inglês
| WPRIM
| ID: wpr-202597
ABSTRACT
Emodin, a naturally occurring anthraquinone derivative isolated from Polygoni cuspidati radix, has several beneficial pharmacologic effects, which include anti-cancer, anti-diabetic, and anti-inflammatory activities. In this study, the authors examined the effect of emodin on the production of proinflammatory cytokines, such as, tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, in mouse bone marrow-derived mast cells (BMMCs) stimulated with phorbol 12-myristate 13-acetate (PMA) plus the calcium ionophore A23187. To investigate the mechanism responsible for the regulation of pro-inflammatory cytokine production by emodin, the authors assessed its effects on the activations of transcriptional factor nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinases (MAPKs). Emodin attenuated the nuclear translocation of (NF)-kappaB p65 and its DNA-binding activity by reducing the phosphorylation and degradation of IkappaBalpha and the phosphorylation of IkappaB kinase B (IKK). Furthermore, emodin dose-dependently attenuated the phosphorylations of MAPKs, such as, extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAP kinase, and the stress-activated protein kinases (SAPK)/c-Jun-N-terminal kinase (JNK). Taken together, the findings of this study suggest that the anti-inflammatory effects of emodin on PMA plus A23187-stimulated BMMCs are mediated via the inhibition of NF-kappaB activation and of the MAPK pathway.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Fosfotransferases
/
Proteínas Quinases
/
Cálcio
/
Citocinas
/
NF-kappa B
/
Calcimicina
/
Emodina
/
Interleucinas
/
Interleucina-6
Limite:
Animais
Idioma:
Inglês
Revista:
Biomolecules & Therapeutics
Ano de publicação:
2013
Tipo de documento:
Artigo
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