Millanvoye-Van Brussel E, Freyss-Beguin M, Homo-Delarche F, Duval D
Inserm U7, Hôpital Necker, Paris, France.
Mol Cell Biochem. 1989;88(1-2):123-7. doi: 10.1007/BF00223433.
We described that oxygen deprivation induced in cultures of heart muscle cells, biochemical events similar to those described in ischemic tissue: arachidonic acid liberation, loss of membrane phospholipids and increase in neutral lipids. Since glucocorticoids have been described to inhibit phospholipase activity and to exert beneficial effects during myocardial infarction, we studied in our experimental model the action of dexamethasone on the metabolism of arachidonic acid and on the synthesis of immunoreactive prostaglandins. Our results show that heart muscle cells produce prostaglandin E2 and 6-keto-prostaglandin-F1 alpha. This synthesis, inhibited by dexamethasone (70% inhibition), decreased after oxygen-deprivation (-45%). The effect of oxygen deprivation and dexamethasone (-60%) are not additive. Moreover, steroid treatment failed to counteract the loss of polyunsaturated fatty acids from the phospholipids, the increase in neutral lipids and the liberation of arachidonic acid induced by oxygen deprivation in muscle cells. These results may indicate that the cardiovascular effects of glucosteroids are not the consequence of a direct effect on heart metabolism at cellular level.
我们描述了在心肌细胞培养中诱导的缺氧情况，其生化事件与缺血组织中所描述的类似：花生四烯酸释放、膜磷脂丢失以及中性脂质增加。由于糖皮质激素已被描述为可抑制磷脂酶活性并在心肌梗死期间发挥有益作用，我们在我们的实验模型中研究了地塞米松对花生四烯酸代谢以及免疫反应性前列腺素合成的作用。我们的结果表明心肌细胞会产生前列腺素E2和6-酮-前列腺素F1α。这种合成受到地塞米松抑制（抑制率70%），在缺氧后下降（-45%）。缺氧和地塞米松的作用（-60%）并非相加性的。此外，类固醇治疗未能抵消缺氧诱导的肌肉细胞中磷脂多不饱和脂肪酸的丢失、中性脂质的增加以及花生四烯酸的释放。这些结果可能表明糖皮质激素对心血管的作用并非细胞水平上对心脏代谢直接作用的结果。
