Sperling R I
Department of Medicine, Harvard Medical School, Boston, Mass.
World Rev Nutr Diet. 1991;66:391-400. doi: 10.1159/000419307.
The studies of dietary fish oil supplementation in healthy volunteers demonstrate: (1) suppression of PMN LTB4 synthesis after a minimum of 4 weeks of dietary fish oil consumption at a level of 4-6 g omega 3 fatty acids daily; concomitant suppression of the other arachidonate-derived 5-lipoxygenase pathway products and decreased [3H]-arachidonic acid release may be observed under certain conditions, (2) suppression of PMN chemotactic responsiveness to LTB4 and FMLP, (3) delayed kinetics of inhibition of chemotaxis and AA metabolism relative to that of cellular lipid alteration, and (4) dietary EPA is more active than DHA in eliciting these effects. The effects of dietary EPA on monocyte function in healthy volunteers include: (1) suppression of LTB4 synthesis concomitantly with that of the other 5-lipoxygenase pathway products and decreased [3H]-arachidonic acid release, (2) suppression of PAF synthesis, and (3) delayed kinetics of inhibition of PAF generation and AA metabolism relative to that of cellular lipid alteration. The effects of dietary fish oil in RA patients include: (1) decreased arachidonate content of cellular lipids with an augmented EPA content, (2) decreased LTB4 generation by PMN as an isolated effect, indicating inhibition of the epoxide hydrolase enzyme. The decrease in LTB4 generation by PMN correlated with improvement of tender joint count in one study, (3) augmentation of depressed PMN chemotaxis to LTB4 and FMLP, and (4) suppression of monocyte PAF generation. From these studies one may conclude that: (1) omega 3 fatty acids are incorporated into leukocyte cellular phospholipids with a concomitant loss in arachidonic acid, (2) the incorporation of omega 3 fatty acids into leukocyte cellular lipids suppresses two pathways of inflammatory mediator synthesis: the 5-lipoxygenase and the PAF synthesis pathways, (3) receptor-mediated PMN functions are altered by dietary omega 3 fatty acid consumption, and (4) these functional changes may be delayed vis-a-vis changes in cellular lipid composition and may vary with the underlying disease states and/or background medication.
（1）每天摄入4 - 6克ω-3脂肪酸，至少4周后可抑制中性粒细胞白三烯B4（LTB4）的合成；在某些情况下，可同时观察到其他花生四烯酸衍生的5-脂氧合酶途径产物的抑制以及[3H]-花生四烯酸释放的减少，（2）抑制中性粒细胞对LTB4和甲酰甲硫氨酸-亮氨酸-苯丙氨酸（FMLP）的趋化反应，（3）相对于细胞脂质改变，趋化性和花生四烯酸（AA）代谢抑制的动力学延迟，以及（4）膳食二十碳五烯酸（EPA）在引发这些效应方面比二十二碳六烯酸（DHA）更具活性。膳食EPA对健康志愿者单核细胞功能的影响包括：（1）与其他5-脂氧合酶途径产物同时抑制LTB4合成以及[3H]-花生四烯酸释放减少，（2）抑制血小板活化因子（PAF）合成，以及（3）相对于细胞脂质改变，PAF生成和AA代谢抑制的动力学延迟。膳食鱼油对类风湿性关节炎（RA）患者的影响包括：（1）细胞脂质中花生四烯酸含量降低，EPA含量增加，（2）中性粒细胞单独产生的LTB4减少，表明环氧水解酶受到抑制。在一项研究中，中性粒细胞产生的LTB4减少与压痛关节计数的改善相关联，（3）增强对LTB4和FMLP反应低下的中性粒细胞趋化性，以及（4）抑制单核细胞PAF生成。从这些研究中可以得出以下结论：（1）ω-3脂肪酸被纳入白细胞细胞磷脂中，同时花生四烯酸含量减少，（2）ω-3脂肪酸纳入白细胞细胞脂质中会抑制炎症介质合成的两条途径：5-脂氧合酶和PAF合成途径，（3）膳食中ω-3脂肪酸的摄入会改变受体介导的中性粒细胞功能，以及（4）相对于细胞脂质组成的变化，这些功能变化可能会延迟，并且可能因潜在疾病状态和/或背景用药而异。
