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首页> 外文期刊>Drug Design, Development and Therapy >Immunomodulatory effects of 17-O-acetylacuminolide in RAW264.7 cells and HUVECs: involvement of MAPK and NF-κB pathways
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Immunomodulatory effects of 17-O-acetylacuminolide in RAW264.7 cells and HUVECs: involvement of MAPK and NF-κB pathways

机译：17-O-乙酰ac啶内酯对RAW264.7细胞和HUVEC的免疫调节作用：MAPK和NF-κB通路的参与

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Abstract: The terpenoid 17-O-acetylacuminolide (AA) was shown to inhibit the production of several inflammatory mediators. However, the mechanisms by which this compound elicited its anti-inflammatory activity remain to be elucidated. In this study, we analyzed the effects of AA on inflammatory gene expression in two different cell types with primordial importance in the inflammatory processes – endothelial cells and macrophages. In human umbilical vein endothelial cells, AA inhibited the expression of inflammatory proteins including the adhesion molecules intercellular adhesion molecule 1; vascular cell adhesion molecule 1; and E-selectin, as well as the release of the chemokine interleukin-8. Additionally, AA hindered the formation of capillary-like tubes in an in vitro model of angiogenesis. AA’s effects in endothelial cells can be attributed at least in part to AA’s inhibition of tumor necrosis factor alpha-induced nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB)’s translocation. Also, in lipopolysaccharide-stimulated macrophage-like RAW264.7 cells, AA was able to downregulate the expression of the genes cyclooxygenase 2, inducible nitric oxide synthase, interleukin-6, and chemokine (C-C motif) ligand 2. Moreover, AA inhibited the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (IκBα), IκB kinase (IKK), and the mitogen-activated protein kinases JNK, ERK, and p38. In conclusion, the present results further support the anti-inflammatory potential of AA in different models of inflammation.
机译：摘要：类萜17-O-乙酰acetyl基内酯（AA）具有抑制多种炎症介质产生的作用。然而，该化合物引发其抗炎活性的机制仍有待阐明。在这项研究中，我们分析了AA对两种在炎症过程中具有重要重要性的细胞类型（内皮细胞和巨噬细胞）中炎症基因表达的影响。在人的脐静脉内皮细胞中，AA抑制炎症蛋白的表达，包括黏附分子细胞间黏附分子1;血管细胞粘附分子1;和E-选择素，以及趋化因子白介素8的释放。另外，AA在体外血管生成模型中阻碍了毛细管样管的形成。机管局对内皮细胞的影响至少可以部分归因于机管局抑制肿瘤坏死因子α诱导的B细胞（NF-κB）易位的kappa轻多肽基因增强子的核因子。此外，在脂多糖刺激的巨噬细胞样RAW264.7细胞中，AA能够下调环氧合酶2，诱导型一氧化氮合酶，白细胞介素6和趋化因子（CC基序）配体2的基因表达。 B细胞抑制剂α（IκBα），IκB激酶（IKK）和促分裂原激活的蛋白激酶JNK，ERK和p38中的κ光多肽基因增强子的核因子磷酸化。总之，本发明结果进一步支持了AA在不同炎症模型中的抗炎潜力。

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