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膳食鱼油和姜黄素联合调节葡聚糖硫酸钠处理小鼠结肠细胞因子动力学和基因表达。

Dietary fish oil and curcumin combine to modulate colonic cytokinetics and gene expression in dextran sodium sulphate-treated mice.

机构信息

Program in Integrative Nutrition and Complex Diseases, Texas A&M University, College Station, TX, USA.

出版信息

Br J Nutr. 2011 Aug;106(4):519-29. doi: 10.1017/S0007114511000390. Epub 2011 Mar 15.

DOI:10.1017/S0007114511000390
PMID:21401974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4422836/
Abstract

Both fish oil (FO) and curcumin have potential as anti-tumour and anti-inflammatory agents. To further explore their combined effects on dextran sodium sulphate (DSS)-induced colitis, C57BL/6 mice were randomised to four diets (2 × 2 design) differing in fatty acid content with or without curcumin supplementation (FO, FO+2 % curcumin, maize oil (control, MO) or MO+2 % curcumin). Mice were exposed to one or two cycles of DSS in the drinking-water to induce either acute or chronic intestinal inflammation, respectively. FO-fed mice exposed to the single-cycle DSS treatment exhibited the highest mortality (40 %, seventeen of forty-three) compared with MO with the lowest mortality (3 %, one of twenty-nine) (P = 0·0008). Addition of curcumin to MO increased (P = 0·003) mortality to 37 % compared with the control. Consistent with animal survival data, following the one- or two-cycle DSS treatment, both dietary FO and curcumin promoted mucosal injury/ulceration compared with MO. In contrast, compared with other diets, combined FO and curcumin feeding enhanced the resolution of chronic inflammation and suppressed (P < 0·05) a key inflammatory mediator, NF-κB, in the colon mucosa. Mucosal microarray analysis revealed that dietary FO, curcumin and FO plus curcumin combination differentially modulated the expression of genes induced by DSS treatment. These results suggest that dietary lipids and curcumin interact to regulate mucosal homeostasis and the resolution of chronic inflammation in the colon.

摘要

鱼油 (FO) 和姜黄素都具有抗肿瘤和抗炎作用。为了进一步探讨它们在葡聚糖硫酸钠 (DSS) 诱导的结肠炎中的联合作用,将 C57BL/6 小鼠随机分为四组饮食 (2×2 设计),在脂肪酸含量上存在差异,分别用或不用姜黄素补充 (FO、FO+2%姜黄素、玉米油 (对照,MO) 或 MO+2%姜黄素)。用饮用水对小鼠进行一次或两次 DSS 暴露,分别诱导急性或慢性肠道炎症。与死亡率最低的 MO(3%,29 只中的 1 只)相比,暴露于单次 DSS 处理的 FO 喂养的小鼠死亡率最高(40%,43 只中的 17 只)(P=0.0008)。与对照相比,MO 中添加姜黄素将死亡率增加到 37%(P=0.003)。与动物存活数据一致,在单次或两次 DSS 处理后,FO 和姜黄素的饮食均与 MO 相比促进了粘膜损伤/溃疡。相比之下,与其他饮食相比,FO 和姜黄素的联合喂养增强了慢性炎症的消退,并抑制了结肠粘膜中关键炎症介质 NF-κB(P<0.05)。粘膜微阵列分析显示,饮食 FO、姜黄素和 FO 加姜黄素联合对 DSS 处理诱导的基因表达有不同的调节作用。这些结果表明,膳食脂质和姜黄素相互作用,调节粘膜内稳态和结肠慢性炎症的消退。

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