A Polysaccharide Isolated from Ecklonia cava Fermented by Lactobacillus brevis Inhibits the Inflammatory Response by Suppressing the Activation of Nuclear Factor-κB in Lipopolysaccharide-Induced RAW 264.7 Macrophages
A Polysaccharide Isolated from Ecklonia cava Fermented by Lactobacillus brevis Inhibits the Inflammatory Response by Suppressing the Activation of Nuclear Factor-κB in Lipopolysaccharide-Induced RAW 264.7 Macrophages
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DOI：
10.1089/jmf.2010.1562
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发表时间：
2011-12-01
影响因子：
2.4
通讯作者：
Jeon, You-Jin
中科院分区：
文献类型：
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作者：
Lee, Won-Woo;Ahn, Ginnae;Jeon, You-Jin
我们先前报道了Viscozyme L（Novozyme Corp.，俄克拉荷马州市，美国）的短乳杆菌发酵的大肠杆菌提取物影响一氧化氮（NO）的产生抑制，这可能与多糖化合物。然而，目前还没有报道多糖的抗炎作用或其生物学机制。在这里，我们研究了多糖的抗炎作用及其在脂多糖（LPS）激活的RAW 264.7细胞的生物学机制。从L.短杆菌发酵E. cava（VLFEP）剂量依赖性地减少LPS刺激的NO产生，而无细胞毒性。而且，VLFEP在100 μ g/mL浓度下显著降低前列腺素E（2）（PGE（2））的产生。此外，VLFEP剂量依赖性地降低诱导型NO合酶的蛋白质和mRNA表达，而它稍微降低环氧合酶2的表达，并且仅在100 μ g/mL浓度下。此外，VLEFP剂量依赖性地降低肿瘤坏死因子-α和白细胞介素-6的生产和/或mRNA表达，与LPS单独刺激的细胞相比。在进一步的实验中，VLFEP显著降低抑制性κ B的磷酸化和降解以及核转录因子-κ B（NF-κ B）p65向核中的移位，并且其DNA结合被LPS刺激显著诱导。本研究表明，VLFEP通过抑制LPS刺激的RAW 264.7细胞中的NF-κ B通路来下调促炎细胞因子和介质的产生和表达，从而发挥抗炎作用。
We previously reported that the increment of carbohydrate content in the Viscozyme (R) L (Novozyme Corp., Oklahoma City, OK, USA) extract of Lactobacillus brevis-fermented Ecklonia cava affected the inhibition of nitric oxide (NO) production and that it might be related to the polysaccharide compound. However, there is no report of anti-inflammatory effects of the polysaccharide or its biological mechanism. Here, we investigated the anti-inflammatory effects of the polysaccharide and its biological mechanism in lipopolysaccharide (LPS)-activated RAW 264.7 cells. The polysaccharide isolated from the Viscozyme extract of L. brevis-fermented E. cava (VLFEP) dose-dependently decreased LPS-stimulated NO production without cytotoxicity. Also, VLFEP significantly decreased the production of prostaglandin E(2) (PGE(2)) at the 100 mu g/mL concentration. In addition, VLFEP dose-dependently decreased the protein and mRNA expressions of inducible NO synthase, whereas it slightly decreased those of cyclooxygenase 2 and only at the 100 mu g/mL concentration. Moreover, VLEFP dose-dependently decreased the productions and/or mRNA expressions of tumor necrosis factor-alpha and interleukin-6, compared with those of LPS only-stimulated cells. In further experiments, VLFEP considerably reduced the phosphorylation and degradation of inhibitory kappa B as well as the translocation of nuclear transcription factor-kappa B (NF-kappa B) p65 into the nucleus, and its DNA binding was markedly induced by LPS stimulation. This study suggests that VLFEP exerts anti-inflammatory effects by down-regulating the production and expression of pro-inflammatory cytokines and mediators via inhibiting the NF-kappa B pathway in LPS-stimulated RAW 264.7 cells.