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多不饱和脂肪酸、炎症过程与炎症性肠病

Polyunsaturated fatty acids, inflammatory processes and inflammatory bowel diseases.

作者信息

Calder Philip C

机构信息

Institute of Human Nutrition, School of Medicine, University of Southampton, Southampton, UK.

出版信息

Mol Nutr Food Res. 2008 Aug;52(8):885-97. doi: 10.1002/mnfr.200700289.

Abstract

With regard to inflammatory processes, the main fatty acids of interest are the n-6 PUFA arachidonic acid (AA), which is the precursor of inflammatory eicosanoids like prostaglandin E(2) and leukotriene B(4), and the n-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA and DHA are found in oily fish and fish oils. EPA and DHA inhibit AA metabolism to inflammatory eicosanoids. They also give rise to mediators that are less inflammatory than those produced from AA or that are anti-inflammatory. In addition to modifying the lipid mediator profile, n-3 PUFAs exert effects on other aspects of inflammation like leukocyte chemotaxis and inflammatory cytokine production. Some of these effects are likely due to changes in gene expression, as a result of altered transcription factor activity. Fish oil has been shown to decrease colonic damage and inflammation, weight loss and mortality in animal models of colitis. Fish oil supplementation in patients with inflammatory bowel diseases results in n-3 PUFA incorporation into gut mucosal tissue and modification of inflammatory mediator profiles. Clinical outcomes have been variably affected by fish oil, although some trials report improved gut histology, decreased disease activity, use of corticosteroids and relapse.

摘要

关于炎症过程,主要涉及的脂肪酸是n-6多不饱和脂肪酸花生四烯酸(AA),它是前列腺素E(2)和白三烯B(4)等炎性类二十烷酸的前体,以及n-3多不饱和脂肪酸二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)。EPA和DHA存在于油性鱼类和鱼油中。EPA和DHA抑制AA代谢生成炎性类二十烷酸。它们还会产生比由AA产生的介质炎症性更低或具有抗炎作用的介质。除了改变脂质介质谱外,n-3多不饱和脂肪酸还对炎症的其他方面产生影响,如白细胞趋化性和炎性细胞因子的产生。其中一些影响可能是由于转录因子活性改变导致基因表达变化所致。在结肠炎动物模型中,鱼油已被证明可减少结肠损伤和炎症、体重减轻及死亡率。对炎性肠病患者补充鱼油会使n-3多不饱和脂肪酸掺入肠道黏膜组织并改变炎性介质谱。尽管一些试验报告称肠道组织学改善、疾病活动度降低、皮质类固醇使用减少及复发减少,但鱼油对临床结局的影响各不相同。

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