炎症是由微生物感染引起的先天免疫应答的主要症状。巨噬细胞,与免疫反应相关的细胞之一,在炎症反应中发挥作用。最近的研究报道各种天然产物可以调节免疫细胞如巨噬细胞的活化。Sargassumhorneri(特纳)C.Agardh是褐藻之一。最近,包括褐藻在内的各种海藻具有抗氧化和抗炎作用。然而,Sargassumhorneri(Turner)C.Agardh的抗炎作用尚不清楚。在这项研究中,我们研究了马尾藻乙醇提取物(Turner)C.Agardh(ESH)对RAW264.7鼠巨噬细胞系的抗炎作用。从干燥的马尾藻(Turner)C中提取ESH。Agardh用70%乙醇提取,然后在-40℃下冻干。ESH对RAW264.7无细胞毒性,通过添加200μg/mLESH,LPS刺激的巨噬细胞激活诱导的一氧化氮(NO)产生显着降低。此外,ESH治疗降低细胞因子的mRNA水平,包括IL-1β,和促炎基因如iNOS和COX-2在LPS刺激的巨噬细胞激活中以剂量依赖的方式。发现ESH通过抑制ERK引起抗炎作用,p-p38和NF-κB磷酸化。此外,ESH抑制LPS刺激的巨噬细胞中IL-1β的释放。这些结果表明,ESH通过抑制ERK对LPS刺激的巨噬细胞活化产生抗炎作用,p-p38,NF-κB,和促炎基因表达。
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 °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 μg/mL of
ESH. Moreover,
ESH treatment reduced mRNA level of cytokines, including IL-1β, 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-κB phosphorylation. In addition,
ESH inhibited the release of IL-1β 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-κB, and pro-inflammatory gene expression.