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肌醇磷脂可能不是星形胶质细胞中类花生酸合成所需花生四烯酸的来源。

Inositol phospholipids are probably not the source of arachidonic acid for eicosanoid synthesis in astrocytes.

作者信息

Pearce B, Jeremy J, Morrow C, Murphy S, Dandona P

出版信息

FEBS Lett. 1987 Jan 19;211(1):73-7. doi: 10.1016/0014-5793(87)81277-2.

Abstract

In astrocyte-enriched cultures of the rat cerebral cortex the Ca2+ ionophore A23187 provoked the breakdown of inositol phospholipids, the liberation of arachidonic acid and the release of prostaglandins E2, F2 alpha, I2 and thromboxane A2. However, agonists for receptors also coupled to inositol phospholipid metabolism in these cells failed to produce an increase in the release of both arachidonic acid and eicosanoids. Results suggest that the A23187-stimulated release of arachidonic acid and eicosanoids is caused by a phospholipase A2-mediated attack on lipids other than the inositol phospholipids. Moreover, receptors linked to inositol lipid turnover are not involved in the control of eicosanoid release from astrocytes.

摘要

在大鼠大脑皮层富含星形胶质细胞的培养物中,钙离子载体A23187引发了肌醇磷脂的分解、花生四烯酸的释放以及前列腺素E2、F2α、I2和血栓素A2的释放。然而,这些细胞中与肌醇磷脂代谢偶联的受体激动剂未能使花生四烯酸和类二十烷酸的释放增加。结果表明,A23187刺激的花生四烯酸和类二十烷酸的释放是由磷脂酶A2介导的对肌醇磷脂以外其他脂质的攻击所致。此外,与肌醇脂质周转相关的受体不参与星形胶质细胞类二十烷酸释放的调控。

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