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鱼油补充剂改变了急性人伤口微环境中炎症脂质介质的水平。

Fish oil supplementation alters levels of lipid mediators of inflammation in microenvironment of acute human wounds.

机构信息

College of Nursing, The Ohio State University, Columbus, Ohio 43210-1289, USA.

出版信息

Wound Repair Regen. 2011 Mar-Apr;19(2):189-200. doi: 10.1111/j.1524-475X.2010.00659.x.

Abstract

Chronic wounds often result from prolonged inflammation involving excessive polymorphonuclear leukocyte activity. Studies show that the ω-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in fish oils generate bioactive lipid mediators that reduce inflammation and polymorphonuclear leukocyte recruitment in numerous inflammatory disease models. This study's purpose was to test the hypotheses that boosting plasma levels of EPA and DHA with oral supplementation would alter lipid mediator levels in acute wound microenvironments and reduce polymorphonuclear leukocyte levels. Eighteen individuals were randomized to 28 days of either EPA+DHA supplementation (Active Group) or placebo. After 28 days, the Active Group had significantly higher plasma levels of EPA (p<0.001) and DHA (p<0.001) than the Placebo Group and significantly lower wound fluid levels of two 15-lipoxygenase products of ω-6 polyunsaturated fatty acids (9-hydroxyoctadecadienoic acid [p=0.033] and 15-hydroxyeicosatrienoic acid [p=0.006]), at 24 hours postwounding. The Active Group also had lower mean levels of myeloperoxidase, a leukocyte marker, at 12 hours and significantly more reepithelialization on Day 5 postwounding. We suggest that lipid mediator profiles can be manipulated by altering polyunsaturated fatty acid intake to create a wound microenvironment more conducive to healing.

摘要

慢性伤口通常是由长期炎症引起的,其中涉及过多的多形核白细胞活性。研究表明,鱼油中的 ω-3 多不饱和脂肪酸二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)产生生物活性脂质介质,可减少多种炎症性疾病模型中的炎症和多形核白细胞募集。本研究的目的是测试以下假设:通过口服补充剂提高 EPA 和 DHA 的血浆水平将改变急性伤口微环境中的脂质介质水平并减少多形核白细胞水平。18 名个体随机分为 28 天的 EPA+DHA 补充剂(活性组)或安慰剂组。28 天后,与安慰剂组相比,活性组的血浆 EPA(p<0.001)和 DHA(p<0.001)水平显著升高,而伤口液中两种 ω-6 多不饱和脂肪酸的 15-脂氧合酶产物(9-羟基十八碳二烯酸[p=0.033]和 15-羟基二十碳三烯酸[p=0.006])水平在受伤后 24 小时显著降低。在受伤后 12 小时,活性组的髓过氧化物酶(白细胞标志物)的平均水平也较低,并且在受伤后第 5 天的上皮再形成明显更多。我们认为,可以通过改变多不饱和脂肪酸的摄入来操纵脂质介质谱,从而创造更有利于愈合的伤口微环境。

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