ABSTRACT Indole-6-carboxaldehyde (I6CA), an indole derivative isolated from the marine brown algae Sargassum thunbergii, is known to have several beneficial effects, but no studies on immune regulation have been conducted. In this study, the immunomodulatory properties of I6CA on murine RAW 264.7 monocyte/macrophage cells were evaluated. As the concentration of I6CA increased, the morphology of RAW 264.7 cells changed to a typical active macrophage shape, and the phagocytic activity increased significantly. I6CA effectively enhanced the production and secretion of immunomodulatory mediators and cytokines due to increased expression of their respective genes. Additionally, I6CA markedly stimulated the expression of Toll-like receptor 4 (TLR4) and its adapter molecule, myeloid differentiation factor 88 (Myd88), and increased TLR4 complexed with Myd88. Furthermore, I6CA promoted the nuclear translocation of nuclear factor-kappa B (NF-κB) by increasing the degradation of the inhibitor of NF-κB-α. Meanwhile, similar trends were also found in lipopolysaccharide-treated cells as a positive control. Furthermore, molecular docking simulation showed that I6CA interacted with TLR4-myeloid differentiation 2 complex. Taken together, the results support the concept that I6CA may increase the activity of the TLR4/NF-κB signaling pathway in order to enhance the immunomodulatory activity of RAW 264.7 cells.

中文翻译：

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从马尾藻 (Mertens) Kuntze 中分离的吲哚-6-甲醛在 RAW 264.7 巨噬细胞中的免疫刺激作用

摘要 Indole-6-carboxaldehyde (I6CA) 是一种从海洋褐藻 Sargassum thunbergii 中分离的吲哚衍生物，已知具有多种有益作用，但尚未对免疫调节进行研究。在这项研究中，评估了 I6CA 对鼠 RAW 264.7 单核细胞/巨噬细胞的免疫调节特性。随着I6CA浓度的增加，RAW 264.7细胞形态转变为典型的活跃巨噬细胞形态，吞噬活性显着增强。由于它们各自基因的表达增加，I6CA 有效地增强了免疫调节介质和细胞因子的产生和分泌。此外，I6CA 显着刺激 Toll 样受体 4 (TLR4) 及其衔接分子髓细胞分化因子 88 (Myd88) 的表达，并增加与 Myd88 复合的 TLR4。此外，I6CA 通过增加 NF-κB-α 抑制剂的降解促进核因子-κB (NF-κB) 的核转位。同时，在作为阳性对照的脂多糖处理的细胞中也发现了类似的趋势。此外，分子对接模拟显示 I6CA 与 TLR4-髓样分化 2 复合物相互作用。总之，结果支持 I6CA 可能增加 TLR4/NF-κB 信号通路的活性以增强 RAW 264.7 细胞的免疫调节活性的概念。分子对接模拟显示 I6CA 与 TLR4-髓样分化 2 复合物相互作用。总之，结果支持 I6CA 可能增加 TLR4/NF-κB 信号通路的活性以增强 RAW 264.7 细胞的免疫调节活性的概念。分子对接模拟显示 I6CA 与 TLR4-髓样分化 2 复合物相互作用。总之，结果支持 I6CA 可能增加 TLR4/NF-κB 信号通路的活性以增强 RAW 264.7 细胞的免疫调节活性的概念。