前列腺素D2通过其环羰基调节人类中性粒细胞的细胞内钙通量并抑制超氧化物释放。

Prostaglandin D2 modulates human neutrophil intracellular calcium flux and inhibits superoxide release via its ring carbonyl.

作者信息

Simpkins C O, Mazorow D L, Alailima S T, Tate E A, Sweatt W, Johnson M, Shariff K, Millar D B

机构信息

Naval Medical Research Institute, Bethesda, Maryland 20814-5055.

出版信息

Life Sci. 1990;46(11):793-801. doi: 10.1016/0024-3205(90)90067-2.

DOI:10.1016/0024-3205(90)90067-2

PMID:2319907

Abstract

We compared the effects of prostaglandin D2 (PGD2), prostaglandin F2 alpha (PGF2) and various ketones on superoxide (OX) release by human neutrophils, which had been stimulated by N-formyl methionyl leucyl phenylalanine (FMLP). Our data suggested that the ring carbonyl of PGD2 is essential to its inhibitory effect on OX release, but the carbonyl group as a ketone, alone is not sufficient. Using the fluorescent Ca2+ probe, Fura-2AM, we found that PGD2 increased the rate of decline of FMLP stimulated intracellular free Ca2+ (Ca)i, but that PGF2 had no effect. cAMP altered FMLP stimulated (Ca)i, in a pattern similar to PGD2. Furthermore, the ring carbonyl of PGD2 is crucial to its effect on OX as well as on (Ca)i.

摘要

我们比较了前列腺素D2（PGD2）、前列腺素F2α（PGF2）和各种酮类对经N-甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）刺激的人中性粒细胞释放超氧化物（OX）的影响。我们的数据表明，PGD2的环羰基对其抑制OX释放的作用至关重要，但单独作为酮的羰基并不足够。使用荧光Ca2+探针Fura-2AM，我们发现PGD2增加了FMLP刺激的细胞内游离Ca2+（Ca）i的下降速率，但PGF2没有作用。环磷酸腺苷（cAMP）以类似于PGD2的模式改变了FMLP刺激的（Ca）i。此外，PGD2的环羰基对其对OX以及对（Ca）i的作用至关重要。