Astragalus polysaccharide induces anti-inflammatory effects dependent on AMPK activity in palmitate-treated RAW264.7 cells
Astragalus polysaccharide induces anti-inflammatory effects dependent on AMPK activity in palmitate-treated RAW264.7 cells
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黄芪多糖在棕榈酸酯处理的 RAW264.7 细胞中诱导依赖于 AMPK 活性的抗炎作用
DOI：
10.3892/ijmm.2013.1335
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发表时间：
2013-06-01
影响因子：
5.4
通讯作者：
He, Xiaohua
中科院分区：
文献类型：
--
作者：
Lu, Jinzhi;Chen, Xiong;He, Xiaohua
黄芪多糖（APS）在动物模型中具有增强胰岛素敏感性和改善糖尿病的作用，研究表明这种作用可能与其在体内和体外的抗炎作用有关。然而，APS在抗炎调节中的潜在药理学机制仍然知之甚少。在此，用APS处理的RAW264.7细胞显示出抗炎作用。黄芪多糖作用24 h后，IL-10蛋白水平及IL-10、巨噬细胞甘露糖受体（MMR）、β-内酰胺酶、Dectin-1、YM-1和YM-2等抗炎基因的表达均显著增加。此外，为了确定APS是否在RAW 264.7细胞炎症中起潜在作用，我们在棕榈酸酯存在下用APS预处理RAW 264.7细胞。结果表明，黄芪多糖能明显恢复棕榈酸对AMPK活性的损伤。此外，APS诱导IL-10蛋白产生和IL-10、MMR、Dectin-1、β-内酰胺酶、YM-1和YM-2的抗炎基因表达。此外，APS抑制IL-1 β蛋白的产生和大多数促炎基因的表达，如IL-1 β、iNOS、MCP-1、IL-6和CD 11 c，但不抑制肿瘤坏死因子（TNF）-α。值得注意的是，当使用DN-AMPK质粒抑制AMPK活性时，APS对炎症基因（TNF-α除外）的作用被消除。这些结果表明，APS通过AMPK活性有效地改善棕榈酸诱导的促炎反应。
Astragalus polysaccharide (APS) has been reported to increase insulin sensitization and to ameliorate diabetes in animal models, and studies have demonstrated that this effect may be correlated with its anti-inflammatory roles in vivo and in vitro. However, the potential pharmacological mechanisms of APS in anti-inflammatory regulation are still poorly understood. Herein, RAW264.7 cells treated with APS showed anti-inflammatory effects. Interleukin (IL)-10 protein levels and expression of most of the anti-inflammatory genes, including IL-10, macrophage mannose receptor (MMR), arginase, Dectin-1, YM-1 and YM-2, were significantly increased after treatment with APS for 24 h. Furthermore, to determine whether APS plays a potential role in RAW264.7 cell inflammation, we pretreated RAW264.7 cells with APS in the presence of palmitate. The results showed that APS markedly recovered the impairment of AMPK activity induced by palmitate. Furthermore, APS induced IL-10 protein production and anti-inflammatory gene expression of IL-10, MMR, Dectin-1, arginase, YM-1 and YM-2. Additionally, APS inhibited IL-1 beta protein production and expression of most of the pro-inflammatory genes, such as IL-1 beta, iNOS, MCP-1, IL-6 and CD11c but not tumor necrosis factor (TNF)-alpha. Notably, the effect of APS on inflammatory genes, except for TNF-alpha, was abrogated when AMPK activity was inhibited using a DN-AMPK plasmid. These results suggest that APS effectively ameliorates palmitate-induced pro-inflammatory responses through AMPK activity.