Dieter P, Schulze-Specking A, Decker K
Eur J Biochem. 1986 Sep 15;159(3):451-7. doi: 10.1111/j.1432-1033.1986.tb09907.x.
Dexamethasone inhibited the stimulus-induced prostaglandin E2 formation by rat Kupffer cells in primary culture, e.g. after treatment with zymosan, phorbol ester, calcium ionophore A23187, platelet-activating factor or lipopolysaccharide. Prostaglandin E2 production from added free arachidonic acid was not influenced by the hormone. The time course, as well as the partial inhibition of the hormone effect by actinomycin D and cycloheximide, point to the hormone-induced formation of a protein which regulates phospholipase A2. The hormone did not affect the phagocytotic activity of the Kupffer cells. The quantity of [3H]arachidonic acid incorporated into phospholipids was also not altered by dexamethasone. After stimulation with zymosan, [3H]arachidonic acid was liberated from phosphatidylcholine only. Superoxide generation by rat Kupffer cells was induced by zymosan, phorbol ester and, to a much smaller extent, by platelet-activating factor. A23187 and lipopolysaccharide were without effect. In contrast to prostaglandin formation, the generation of superoxide was not influenced by dexamethasone. These results indicate that in cultured rat Kupffer cells prostaglandin formation and superoxide generation are independently triggered processes.
地塞米松抑制原代培养的大鼠枯否细胞受刺激诱导的前列腺素E2生成，例如在用酵母聚糖、佛波酯、钙离子载体A23187、血小板活化因子或脂多糖处理后。激素对由添加的游离花生四烯酸产生前列腺素E2没有影响。时间进程以及放线菌素D和环己酰亚胺对激素作用的部分抑制表明，激素诱导形成一种调节磷脂酶A2的蛋白质。激素不影响枯否细胞的吞噬活性。地塞米松也不改变掺入磷脂中的[3H]花生四烯酸的量。在用酵母聚糖刺激后，[3H]花生四烯酸仅从磷脂酰胆碱中释放出来。大鼠枯否细胞的超氧化物生成由酵母聚糖、佛波酯诱导，血小板活化因子在较小程度上诱导。A23187和脂多糖没有作用。与前列腺素形成相反，超氧化物的生成不受地塞米松影响。这些结果表明，在培养的大鼠枯否细胞中，前列腺素形成和超氧化物生成是独立触发的过程。
