Zhang C L, Lyngmo V, Nordøy A
Department of Medicine, University of Tromsø, Norway.
Thromb Res. 1992 Jan 1;65(1):65-75. doi: 10.1016/0049-3848(92)90226-z.
The present study reports on the effects of myristic(14:0), palmitic(16:0) and stearic(18:0) acids separately and combined with linoleic(18:2n-6), arachidonic(20:4n-6) and eicosapentaenoic(20:5n-3) acids on cultured human endothelial cell monolayers(ECM). The cell viability determined by trypan blue exclusion study, the release of lactate dehydrogenase(LDH) and 6-keto-PGF1 alpha into the medium from ECM incubated with albumin bound fatty acids(FA) were measured. The cell viability was reduced and the release of LDH from ECM was enhanced by 18:0(0.2mM, ratio 1, 2 and 4) and 16:0(0.4mM, ratio 2), but not by 14:0, or the unsaturated FA. The reduced cell viability induced by 18:0 was completely inhibited by polyunsaturated FA, 18:2n-6, 20:4n-6 and 20:5n-3. The release of 6-keto-PGF1 alpha was increased by 18:0, but not by 14:0 and 16:0. All three saturated FA potentiated 6-keto-PGF1 alpha production induced by 20:4n-6. Combined with 18:2n-6 or 20:5n-3, they also stimulated 6-keto-PGF1 alpha production. This study indicates that the three main dietary SFA, 18:0, 16:0 and 14:0 do not have the same effects on ECM. The damaging effect on endothelial cells induced by 18:0 and 16:0 may be of significance for the thrombogenic effects related to these saturated fatty acids.
本研究报告了肉豆蔻酸（14:0）、棕榈酸（16:0）和硬脂酸（18:0）分别以及与亚油酸（18:2n - 6）、花生四烯酸（20:4n - 6）和二十碳五烯酸（20:5n - 3）联合使用时，对培养的人内皮细胞单层（ECM）的影响。通过台盼蓝排斥试验测定细胞活力，测量与白蛋白结合脂肪酸（FA）孵育的ECM向培养基中释放乳酸脱氢酶（LDH）和6 - 酮 - PGF1α的情况。18:0（0.2mM，比例1、2和4）和16:0（0.4mM，比例2）会降低细胞活力并增强ECM中LDH的释放，但14:0或不饱和脂肪酸不会。18:0诱导的细胞活力降低被多不饱和脂肪酸18:2n - 6、20:4n - 6和20:5n - 3完全抑制。18:0会增加6 - 酮 - PGF1α的释放，但14:0和16:0不会。所有三种饱和脂肪酸都增强了20:4n - 6诱导的6 - 酮 - PGF1α的产生。与18:2n - 6或20:5n - 3联合使用时，它们也会刺激6 - 酮 - PGF1α的产生。本研究表明，三种主要的膳食饱和脂肪酸18:0、16:0和14:0对ECM的影响并不相同。18:0和16:0对内皮细胞的损伤作用可能与这些饱和脂肪酸的血栓形成作用有关。
