Activation of RAW264.7 macrophages by the polysaccharide from the roots of Actinidia eriantha and its molecular mechanisms

Activation of RAW264.7 macrophages by the polysaccharide from the roots of Actinidia eriantha and its molecular mechanisms
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毛花猕猴桃根多糖激活RAW264.7巨噬细胞及其分子机制

DOI:
10.1016/j.carbpol.2014.12.023
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发表时间:
2015-05-05
影响因子:
11.2
通讯作者:
Wang, Hui
Wang, Hui
中科院分区:
化学1区
文献类型:
--
作者:
Sun, Hongxiang;Zhang, Juan;Wang, Hui

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毛花猕猴桃 (AEPS) 根中的多糖是一种有效的抗肿瘤剂和免疫佐剂,研究人员研究了其对 RAW264.7 巨噬细胞的免疫调节作用及其分子机制。 AEPS可显着增强RAW264.7细胞的胞饮和吞噬活性,诱导NO、TNF-α、IL-10、IL-1β和IL-6的产生,促进辅助分子和共刺激分子的表达。 PCR阵列检测显示,AEPS上调了28个基因,包括TLR(TLR2、TLR8、TLR9)、促炎因子(IL-1β、G-CSF、IL-1α、GM-CSF、IL-6、COX-2、TNF-α、IFN-β、CXCL10、CCL2、TNF-β、IL-10)以及NF-κB信号通路相关基因,并下调TLR3、TLR4、PGLYRP1、EIF2 α K2、MAP3K1 和 IRF1 等 6 个基因。进一步显示 AEPS 可促进 RAW264.7 细胞中细胞质 I kappa B-alpha 降解并增加核 NF-kappa B p65 水平。这些结果表明,AEPS 激活 RAW264.7 巨噬细胞,并通过 TLRs/NF-kappa B 信号通路引发 M1 和 M2 反应。 (C) 2014 Elsevier Ltd. 保留所有权利。
The polysaccharide from the roots of Actinidia eriantha (AEPS), a potent antitumor agent and immunological adjuvant, was investigated for the immunomodulatory effects on RAW264.7 macrophages and its molecular mechanisms. AEPS could significantly enhance the pinocytic and phagocytic activity, induce the production of NO, TNF-alpha, IL-10, IL-1 beta and IL-6, and promote the expression of accessory and costimulatory molecules in RAW264.7 cells. PCR array assay revealed that AEPS up-regulated 28 genes including TLRs (TLR2, TLR8, TLR9), proinflammatory factors (IL-1 beta, G-CSF, IL-1 alpha, GM-CSF, IL-6, COX-2, TNF-alpha, IFN-beta, CXCL10, CCL2, TNF-beta, IL-10), and the genes involved in NF-kappa B signaling pathway, and down-regulated 6 genes such as TLR3, TLR4, PGLYRP1, EIF2 alpha K2, MAP3K1 and IRF1. AEPS was further showed to promote cytoplasmic I kappa B-alpha degradation and increase nuclear NF-kappa B p65 levels in RAW264.7 cells. These results suggested that AEPS activated RAW264.7 macrophages and elicited a M1 and M2 response through TLRs/NF-kappa B signaling pathway. (C) 2014 Elsevier Ltd. All rights reserved.