Kim D N, Schmee J, Lee C S, Solis O, Ross J S, Thomas W A
Department of Pathology and Laboratory Medicine, Albany Medical College, New York 12208.
Exp Mol Pathol. 1991 Aug;55(1):1-12. doi: 10.1016/0014-4800(91)90013-n.
We have reported previously that fish oil rich in omega-3 fatty acids added to a butter-cholesterol atherogenic diet for swine resulted in marked retardation of the atherosclerotic process which many regard as largely an inflammatory response to injury by excessive lipids in the intima. In this report on the same swine we present serum levels of several eicosanoids derived from arachidonic acid via the cyclooxygenase and lipoxygenase pathways. The study involves six swine fed a high fat, high cholesterol diet (BT group) for 4 months, six swine fed the same diet but with 30 ml/day fish oil added (BT + FO), and five swine fed a low fat, low cholesterol mash diet (MA). The serum eicosanoids were measured by radioimmunoassay. Thromboxane B2 levels (ng/dl: means +/- SEM) were 543 +/- 49 for MA, 231 +/- 12 for BT, and 105 +/- 20 for BT + FO, and all differences were statistically highly significant, 6-Keto PGF1 alpha (a relatively stable prostacyclin metabolite) levels were 249 +/- 31 for MA, 184 +/- 12 for BT, and 101 +/- 10 for BT + FO, and all differences were significant. Leukotriene B4 levels at 4 months were 151 +/- 25 for MA, 112 +/- 11 for BT, and 84 +/- 11 for BT + FO. BT + FO was significantly different from both MA and BT, but BT was not significantly different from MA. Leukotriene C4 levels were not significantly different among the three groups. Of special interest was the effect of the BT diet without the FO additive in reducing several eicosanoid levels compared to MA values. The affected eicosanoid levels were reduced still further by the fish oil additive, indicating its ability to inhibit both the cyclooxygenase and the lipoxygenase pathways. The relation of the fish oil-induced inhibition to the observed retardation of atherogenesis is not as yet clear but there are several theoretical possibilities, including reduction in recruitment of monocytes and in proliferation of smooth muscle cells.
我们之前曾报道，在猪的黄油 - 胆固醇致动脉粥样化饮食中添加富含ω-3脂肪酸的鱼油，会导致动脉粥样硬化进程显著减缓，许多人认为这一进程在很大程度上是内膜中过量脂质引发的炎症反应。在这份关于同一批猪的报告中，我们展示了通过环氧化酶和脂氧合酶途径从花生四烯酸衍生而来的几种类花生酸的血清水平。该研究涉及六只猪，它们被喂食高脂肪、高胆固醇饮食（BT组）4个月；六只猪被喂食相同饮食，但每天添加30毫升鱼油（BT + FO组）；还有五只猪被喂食低脂、低胆固醇混合饲料（MA组）。血清类花生酸通过放射免疫测定法进行测量。血栓素B2水平（纳克/分升：均值±标准误），MA组为543±49，BT组为231±12，BT + FO组为105±20，所有差异在统计学上都具有高度显著性；6 - 酮 - PGF1α（一种相对稳定的前列环素代谢物）水平，MA组为249±31，BT组为184±12，BT + FO组为101±10，所有差异均具有显著性。4个月时白三烯B4水平，MA组为151±25，BT组为112±11，BT + FO组为84±11。BT + FO组与MA组和BT组均有显著差异，但BT组与MA组无显著差异。三组之间白三烯C4水平无显著差异。特别值得关注的是，与MA组相比，不含鱼油添加剂的BT饮食对降低几种类花生酸水平的影响。鱼油添加剂进一步降低了受影响的类花生酸水平，表明其能够抑制环氧化酶和脂氧合酶途径。鱼油诱导的抑制作用与观察到的动脉粥样硬化形成减缓之间的关系尚不清楚，但存在几种理论可能性，包括单核细胞募集减少和平滑肌细胞增殖减少。
