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Inhibitory Effect of Octylcaffeate on Lipopolysaccharide-Induced Nitric Oxide Production in Macrophages

机译:咖啡酸辛酯对脂多糖诱导的巨噬细胞一氧化氮产生的抑制作用

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摘要

We have investigated the effect of octylcaffeate on lipopolysaccharide-induced nitric oxide production in a macrophage-derived cell line, RAW 264.7. Octyl-caffeate (0.1, 0.5, 0.8 and 1muM) inhibited the production in a concentration-dependent manner when treated simultaneously with LPS (1mu g/mL) . Treatment of octylcaffeate (1mu M) between 2 h before and 1h after the treatment of LPS was found to be effective, but the protective efficacy of octylcaffeate was diminishted when given before or after this time interval. Octylcaffeate (0.055 0.1,0.5 and 0.8 mu M) also inhibited the protein expression of inducible nitric oxide synthase. These results suggest that octylcaffeate attenuates lipopolysaccharide-stimulated expression of nitric oxide synthase in macrophages which may help to explain the antiinflammatory actions of this compound.
机译:我们已经研究了辛基咖啡酸酯对巨噬细胞衍生的细胞系RAW 264.7中脂多糖诱导的一氧化氮生成的影响。当同时用LPS(1μg/ mL)处理时,咖啡酸辛酯(0.1、0.5、0.8和1μM)以浓度依赖的方式抑制了生产。 LPS治疗前2小时至治疗后1小时之间,咖啡因辛酯(1μM)被认为是有效的,但是在该时间间隔之前或之后给予辛基咖啡因的保护作用减弱。咖啡酸辛酯(0.055 0.1、0.5和0.8μM)也抑制诱导型一氧化氮合酶的蛋白质表达。这些结果表明,咖啡酸辛酯减弱了脂多糖刺激的巨噬细胞中一氧化氮合酶的表达,这可能有助于解释该化合物的抗炎作用。

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