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首页> 外文期刊>Journal of Agricultural and Food Chemistry >Anti-inflammatory Activities of an Ethanol Extract of Ecklonia stolonifera in Lipopolysaccharide-Stimulated RAW 264.7 Murine Macrophage Cells
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Anti-inflammatory Activities of an Ethanol Extract of Ecklonia stolonifera in Lipopolysaccharide-Stimulated RAW 264.7 Murine Macrophage Cells

机译:链球菌乙醇提取物在脂多糖刺激的RAW 264.7鼠巨噬细胞中的抗炎活性

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摘要

Ecklonia stolonifera is a brown alga that was shown to have antioxidant, anti-inflammatory, tyrosinase inhibitory, and chemopreventive activities, However, the molecular mechanisms underlying its anti-inflammatory activity remain unclear. In this study, we investigated the molecular mechanism of the anti-inflammatory action of B. stolonifera ethanolic extracts (ESE) using lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. ESE inhibited LPS-induced nitric oxide (IC_(50) = 72 ± 1.9 μg/mL) and prostaglandin E2 (IC_(50) = 98 ± 5.3 μg/mL) production in a dose-dependent manner and suppressed the expression of inducible nitric oxide synthase and cyclooxygenase-2 in RAW 264.7 cells. ESE also reduced the production of pro-inflammatory cytokines in LPS-stimulated RAW 264.7 cells. LPS-induced nuclear factor-kB (NF-kB) transcriptional activity and NF-kB translocation into the nucleus were significantly inhibited by ESE treatment through the prevention of the degradation of inhibitor kB-α, Moreover, ESE inhibited the activation of Akt, ERK, JNK1/2, and p38 MAPK in LPS-stimulated RAW 264.7 cells. The main components with anti-inflammatory activity in ESE were identified as phlorofucofuroeckol A and B based on the inhibition of NO production. Our results indicate that ESE can be considered as a potential source of therapeutic agents for inflammatory diseases.
机译:Ecklonia stolonifera是一种褐藻,被证明具有抗氧化,抗炎,酪氨酸酶抑制和化学预防活性,然而,其抗炎活性的分子机制仍不清楚。在这项研究中,我们调查了脂多糖(LPS)刺激的RAW 264.7细胞对stostoifera乙醇提取物(ESE)抗炎作用的分子机制。 ESE以剂量依赖性方式抑制LPS诱导的一氧化氮(IC_(50)= 72±1.9μg/ mL)和前列腺素E2(IC_(50)= 98±5.3μg/ mL)的产生,并抑制诱导型一氧化氮的表达。 RAW 264.7细胞中的氧化合酶和环加氧酶-2。 ESE还减少了LPS刺激的RAW 264.7细胞中促炎性细胞因子的产生。通过ESE处理,通过防止抑制剂kB-α的降解,LPS诱导的核因子-kB(NF-kB)转录活性和NF-kB易位进入核内,此外,ESE抑制了Akt,ERK的活化,LPS刺激的RAW 264.7细胞中的JNK1 / 2和p38 MAPK。基于抑制NO产生,在ESE中具有抗炎活性的主要成分被鉴定为phofofucofuroeckol A和B。我们的结果表明,ESE可被视为炎症性疾病治疗剂的潜在来源。

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