Blockade of TGF-ß-activated kinase 1 prevents advanced glycation end products-induced inflammatory response in macrophages.
Cytokine
; 78: 62-8, 2016 Feb.
Article
em En
| MEDLINE
| ID: mdl-26687627
ABSTRACT
Advanced glycation end products (AGEs), inflammatory-activated macrophages are essential in the initiation and progression of diabetic nephropathy (DN). TGF-ß-activated kinase 1 (TAK1) plays a vital role in innate immune responses and inflammation. However, little information has been available about the effects of AGEs on the regulation of TAK1 expression and underlying mechanisms in AGEs-stimulated macrophage activation. We hypothesized TAK1 signal pathway in AGEs conditions could be a vital factor contributing to macrophage activation and inflammation. Thus, in the present study, we used bone marrow-derived macrophages (BMMs) to explore the functional role and potential mechanisms of TAK1 pathway under AGEs conditions. Results indicated that TAK1 played important roles in AGEs-induced mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B protein (NF-κB) activation, which regulated the production of monocyte chemo-attractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) in AGEs-stimulated macrophages. The results also suggested that TAK1 inhibitor (5Z-7-oxozeaenol) could inhibit AGEs-induced macrophage activation to down-regulate inflammatory cytokine production via MAPKs and NF-κB pathways, indicating that 5Z-7-oxozeaenol might be an immunoregulatory agent against AGEs-stimulated inflammatory response in DN.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Produtos Finais de Glicação Avançada
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MAP Quinase Quinase Quinases
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Ativação de Macrófagos
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Macrófagos
Limite:
Animals
Idioma:
En
Ano de publicação:
2016
Tipo de documento:
Article