Fujimoto Y, Uno H, Kagen C, Ueno T, Fujita T
Biochem J. 1985 Dec 15;232(3):625-8. doi: 10.1042/bj2320625.
The effect of diarachidonin on the synthesis of prostaglandin E2 in rabbit kidney medulla slices was examined. The addition of diarachidonin stimulated prostaglandin E2 production in a dose-dependent manner. At three concentrations (10, 50 and 100 microM), increases in prostaglandin E2 formation induced by exogenous diarachidonin were 2-fold greater than those induced by exogenous arachidonic acid. Diacylglycerol or phosphatidic acid from egg lecithin had little or no effect on prostaglandin E2 production. Moreover, EGTA failed to inhibit diarachidonin-stimulated prostaglandin E2 formation, indicating that the stimulatory effect of diarachidonin is not mediated through the activation of endogenous phospholipase A2 (including phosphatidic acid-specific phospholipase A2). These results are discussed in the light of our former hypothesis that arachidonic acid release from kidney medulla phospholipids might occur through the sequential action of a phospholipase C coupled to diacylglycerol and monoacylglycerol lipases [Fujimoto, Akamatsu, Hattori & Fujita (1984) Biochem. J. 218, 69-74].
研究了二花生四烯酸甘油酯对兔肾髓质切片中前列腺素E2合成的影响。添加二花生四烯酸甘油酯以剂量依赖的方式刺激前列腺素E2的产生。在三个浓度（10、50和100微摩尔）下，外源性二花生四烯酸甘油酯诱导的前列腺素E2生成增加量比外源性花生四烯酸诱导的增加量高2倍。来自卵磷脂的二酰基甘油或磷脂酸对前列腺素E2的产生几乎没有影响。此外，乙二醇双四乙酸（EGTA）未能抑制二花生四烯酸甘油酯刺激的前列腺素E2生成，这表明二花生四烯酸甘油酯的刺激作用不是通过内源性磷脂酶A2（包括磷脂酸特异性磷脂酶A2）的激活介导的。根据我们之前的假设，即肾髓质磷脂中的花生四烯酸释放可能通过与二酰基甘油和单酰基甘油脂肪酶偶联的磷脂酶C的顺序作用发生，对这些结果进行了讨论[藤本、赤松、服部和藤田（1984年）《生物化学杂志》218卷，69 - 74页]。
