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从葡萄糖-赖氨酸美拉德反应模型体系中回收的生物活性馏分的抗氧化和抗炎活性的表征。

Characterization of antioxidant and anti-inflammatory activities of bioactive fractions recovered from a glucose-lysine Maillard reaction model system.

机构信息

Food, Nutrition, and Health, Faculty of Land and Food Systems, University of British Columbia, 2205 East Mall, Vancouver, BC V6T 1Z4, Canada.

出版信息

Mol Cell Biochem. 2012 May;364(1-2):147-57. doi: 10.1007/s11010-011-1213-7. Epub 2012 Jan 11.

Abstract

A glucose-lysine (Glu-Lys) Maillard reaction mixture heated at 121°C for 60 min was processed by ultrafiltration, ethyl acetate extraction, and semi-preparative HPLC to recover a bioactive fraction, termed F3. F3, characterized by spectral analysis to contain three distinct components, inhibited NO and IL-8 by 70 and 61%, respectively, at a concentration of 50 μg/ml in inflamed Caco-2 cells induced by IFN-γ and phorbol 12-myristate 13-acetate (PMA). F3 significantly (P < 0.05) down-regulated several genes involved in nuclear factor kappa B (NF-κB) signaling pathway. These genes included the cytokine receptors, TNFRSF10A and TNFRSF10B; receptor-associated proteins, IRAK2 and TICAM1; the inhibitor κB kinase, IKBKE; the NF-κB inhibitor, NFKBIA; and the NF-κB subunits, REL, RELA, and RELB. F3 also down-regulated the NF-κB responsive genes IL-8, NOS2, and ICAM1, attenuated the gene expression of peroxidases such as DUOX1 and DUOX2, and relieved the down-regulated GCFHR that are involved in the biosynthesis of NO and TROAP, a gene suppressed by NO. The anti-inflammatory activity of F3 was mediated through multiple processes that included regulation of gene expressions involved in NF-κB signaling, the inhibition of IL-8 and iNOS translation, a decrease in NO synthesis and attenuating oxidative stress in inflamed Caco-2 cells. Our results show that MRP components have the potential to suppress inflammation in IFN-γ and PMA-induced Caco-2 cells.

摘要

葡萄糖-赖氨酸(Glu-Lys)美拉德反应混合物在 121°C 下加热 60 分钟,通过超滤、乙酸乙酯萃取和半制备 HPLC 进行处理,以回收具有生物活性的部分,称为 F3。F3 通过光谱分析鉴定为含有三个不同的成分,在浓度为 50μg/ml 时,分别抑制了由 IFN-γ和佛波醇 12-肉豆蔻酸 13-乙酸酯(PMA)诱导的炎症 Caco-2 细胞中的 NO 和 IL-8,抑制率分别为 70%和 61%。F3 显著(P<0.05)下调了几个参与核因子 kappa B(NF-κB)信号通路的基因。这些基因包括细胞因子受体 TNFRSF10A 和 TNFRSF10B;受体相关蛋白 IRAK2 和 TICAM1;NF-κB 抑制剂激酶 IKBKE;NF-κB 抑制剂 NFKBIA;以及 NF-κB 亚基 REL、RELA 和 RELB。F3 还下调了 NF-κB 反应基因 IL-8、NOS2 和 ICAM1,减弱了过氧化物酶如 DUOX1 和 DUOX2 的基因表达,并缓解了参与 NO 和 TROAP 生物合成的 GCFHR 的下调,NO 抑制了 TROAP 的表达。F3 的抗炎活性是通过多种途径介导的,包括调节 NF-κB 信号通路相关基因的表达,抑制 IL-8 和 iNOS 的翻译,减少 NO 的合成,减轻炎症 Caco-2 细胞中的氧化应激。我们的结果表明,MRP 成分具有抑制 IFN-γ和 PMA 诱导的 Caco-2 细胞炎症的潜力。

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