Anti-inflammatory Effects of Ethanolic Extract from Sargassum horneri (Turner) C. Agardh on Lipopolysaccharide-Simulated Macrophage Activation via NF-κB Pathway Regulation
Anti-inflammatory Effects of Ethanolic Extract from Sargassum horneri (Turner) C. Agardh on Lipopolysaccharide-Simulated Macrophage Activation via NF-κB Pathway Regulation
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DOI：
10.3109/08820139.2014.942459
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发表时间：
2015-01-01
影响因子：
2.8
通讯作者：
Lee, Jun Sik
中科院分区：
文献类型：
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作者：
Kim, Mi Eun;Jung, Yun Chan;Lee, Jun Sik
炎症是微生物感染引起的先天免疫反应的主要症状。巨噬细胞是免疫反应相关细胞之一，在炎症反应中发挥作用。最近的研究表明，多种天然产物可以调节巨噬细胞等免疫细胞的活化。马尾藻 (Turner) C. Agardh 是褐藻之一。近年来，包括褐藻在内的多种海藻具有抗氧化和抗炎作用。然而，马尾藻的抗炎作用仍不清楚。在本研究中，我们研究了马尾藻乙醇提取物 (ESH) 对 RAW 264.7 小鼠巨噬细胞系的抗炎作用。 ESH 是用 70% 乙醇从干燥的马尾藻 (Turner) C. Agardh 中提取的，然后在 -40°C 下冻干。ESH 对 RAW 264.7 没有细胞毒性，并且添加 200 mg/mL ESH 后，由 LPS 刺激的巨噬细胞活化诱导的一氧化氮 (NO) 产生显着减少。此外，ESH 治疗以剂量依赖性方式降低 LPS 刺激的巨噬细胞活化中细胞因子（包括 IL-1β）和促炎基因（如 iNOS 和 COX-2）的 mRNA 水平。研究发现 ESH 通过抑制 ERK、p-p38 和 NF-kappa B 磷酸化来引发抗炎作用。此外，ESH 抑制 LPS 刺激的巨噬细胞中 IL-1b 的释放。这些结果表明，ESH 通过抑制 ERK、p-p38、NF-κ B 和促炎基因表达，对 LPS 刺激的巨噬细胞活化产生抗炎作用。
Inflammation is major symptom of the innate immune response by infection of microbes. Macrophages, one of immune response related cells, play a role in inflammatory response. Recent studies reported that various natural products can regulate the activation of immune cells such as macrophage. Sargassum horneri (Turner) C. Agardh is one of brown algae. Recently, various seaweeds including brown algae have antioxidant and anti-inflammatory effects. However, anti-inflammatory effects of Sargassum horneri (Turner) C. Agardh are still unknown. In this study, we investigated anti-inflammatory effects of ethanolic extract of Sargassum horneri (Turner) C. Agardh (ESH) on RAW 264.7 murine macrophage cell line. The ESH was extracted from dried Sargassum horneri (Turner) C. Agardh with 70% ethanol and then lyophilized at -40 degrees C. ESH was not cytotoxic to RAW 264.7, and nitric oxide (NO) production induced by LPS-stimulated macrophage activation was significantly decreased by the addition of 200 mg/mL of ESH. Moreover, ESH treatment reduced mRNA level of cytokines, including IL-1 beta, and pro-inflammatory genes such as iNOS and COX-2 in LPS-stimulated macrophage activation in a dose-dependent manner. ESH was found to elicit anti-inflammatory effects by inhibiting ERK, p-p38 and NF-kappa B phosphorylation. In addition, ESH inhibited the release of IL-1b in LPS-stimulated macrophages. These results suggest that ESH elicits anti-inflammatory effects on LPS-stimulated macrophage activation via the inhibition of ERK, p-p38, NF-kappa B, and pro-inflammatory gene expression.