Lippiello L
Department of Orthopaedic Surgery, University of Nebraska Medical Center, Omaha 68198.
Proc Soc Exp Biol Med. 1990 Nov;195(2):282-7. doi: 10.3181/00379727-195-43149.
Observations of impaired chondrocyte metabolism in essential fatty acid (EFA) deficiency as well as EFA protection against development of osteoarthrosis in inbred mice suggest the existence of a relationship between EFA, chondrocyte metabolism, and cartilage degeneration. To explore this relationship further, the fatty acid content of lipids in normal fetal bovine chondrocytes was manipulated by in vitro exposure to media supplemented with 100 microM arachidonic acid (20:4) or oleic acid (18:1). Chondrocytes rapidly and differentially incorporated both fatty acids into their lipid pools. The predominant acceptor was triacylglycerols. A 980% enrichment of arachidonic acid was associated with increased concentrations of fatty acids, increased 35SO4 and [3H]proline incorporation into matrix macromolecules (170% and 54-103%, respectively), and a 24-fold elevation in chondrocyte prostaglandin synthesis. No metabolic effects elicited observed in cells enriched by 377% with 18:1 oleic acid. The metabolic effects elicited by 20:4 arachidonic acid were abolished by pretreatment of cells with indomethacin, suggesting that the cellular responses to essential fatty acid loading may be associated with induced increases in prostaglandin synthesis. The data indicate that excessive in vitro accumulation of arachidonic acid is associated with an increase in synthetic activity that is causally related to increased prostaglandin synthesis and elevated levels of cellular fatty acids.
对必需脂肪酸(EFA)缺乏时软骨细胞代谢受损以及EFA对近交系小鼠骨关节炎发展具有保护作用的观察结果表明,EFA、软骨细胞代谢和软骨退变之间存在关联。为了进一步探究这种关系,通过体外将正常胎牛软骨细胞暴露于添加了100微摩尔花生四烯酸(20:4)或油酸(18:1)的培养基中,来操控脂质中的脂肪酸含量。软骨细胞迅速且有差异地将这两种脂肪酸纳入其脂质库。主要的接受体是三酰甘油。花生四烯酸980%的富集与脂肪酸浓度增加、基质大分子中35SO4和[3H]脯氨酸掺入量增加(分别为170%和54 - 103%)以及软骨细胞前列腺素合成增加24倍相关。在富含377%的18:1油酸的细胞中未观察到代谢效应。用吲哚美辛预处理细胞可消除20:4花生四烯酸引发的代谢效应,这表明细胞对必需脂肪酸负荷的反应可能与诱导的前列腺素合成增加有关。数据表明,体外花生四烯酸的过度积累与合成活性增加相关,而合成活性增加与前列腺素合成增加和细胞脂肪酸水平升高存在因果关系。