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Blockade of TGF-beta-activated kinase 1 prevents advanced glycation end products-induced inflammatory response in macrophages

机译:TGF-β激活激酶1的阻止阻止巨噬细胞中晚期糖基化终产物诱导的炎症反应

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Advanced glycation end products (AGEs), inflammatory-activated macrophages are essential in the initiation and progression of diabetic nephropathy (DN). TGF-beta-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-kappa B) activation, which regulated the production of monocyte chemo-attractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) 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-kappa B pathways, indicating that 5Z-7-oxozeaenol might be an immunoregulatory agent against AGEs-stimulated inflammatory response in DN. (C) 2015 Elsevier Ltd. All rights reserved.
机译:晚期糖基化终产物(AGEs),炎症激活的巨噬细胞在糖尿病性肾病(DN)的发生和发展中至关重要。 TGF-beta激活的激酶1(TAK1)在先天免疫反应和炎症中起着至关重要的作用。但是,关于AGEs对TAK1表达的调节作用以及AGEs刺激巨噬细胞激活的潜在机制的信息很少。我们假设AGEs条件下的TAK1信号通路可能是促成巨噬细胞活化和炎症的重要因素。因此,在本研究中,我们使用了骨髓源性巨噬细胞(BMM)来探索AGEs条件下TAK1途径的功能作用和潜在机制。结果表明,TAK1在AGEs诱导的促分裂原活化蛋白激酶(MAPK)和核因子κB蛋白(NF-κB)活化中起重要作用,从而调节单核细胞趋化蛋白1(MCP-1)的产生。和AGEs刺激的巨噬细胞中的肿瘤坏死因子-α(TNF-alpha)。结果还表明TAK1抑制剂(5Z-7-oxozeaenol)可以抑制AGEs诱导的巨噬细胞活化,从而通过MAPK和NF-κB途径下调炎性细胞因子的产生,表明5Z-7-oxozeaenol可能是针对AGEs刺激DN中的炎症反应。 (C)2015 Elsevier Ltd.保留所有权利。

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