环孢素对前列环素生成的抑制作用并非由于培养的人内皮细胞膜磷脂中花生四烯酸的可用性降低所致。

Inhibition of prostacyclin formation by cyclosporin is not due to reduced availability of arachidonic acid in membrane phospholipids of cultured human endothelial cells.

作者信息

Brown Z, Neild G H, Lewis G P

机构信息

Department of Renal Medicine, Institute of Urology, St Paul's Hospital, London, U.K.

出版信息

Biochem Pharmacol. 1990 Mar 15;39(6):1136-8. doi: 10.1016/0006-2952(90)90295-v.

DOI:10.1016/0006-2952(90)90295-v

PMID:2108684

Abstract

Our studies have shown that CS inhibits PGI2 production in HUVEC, that this inhibition is not overcome when exogenous AA is supplied, that the inhibitory action of CS is proximal to PGI2 synthetase and finally that there is abundant free AA available in membrane phospholipids of CS treated HUVEC [4,5]. In conclusion, CS does not appear to inhibit PGI2 synthesis by reducing the availability of free AA in the endothelial cell membrane. Although CS appears to inhibit cyclo-oxygenase, we can not exclude an additional effect on acyltransferase.

摘要

我们的研究表明，氯沙坦（CS）可抑制人脐静脉内皮细胞（HUVEC）中前列环素（PGI2）的生成；当提供外源性花生四烯酸（AA）时，这种抑制作用无法被克服；CS的抑制作用发生在PGI2合成酶的上游；最后，经CS处理的HUVEC细胞膜磷脂中有大量游离AA[4,5]。总之，CS似乎并非通过减少内皮细胞膜中游离AA的可利用性来抑制PGI2的合成。尽管CS似乎可抑制环氧化酶，但我们不能排除其对酰基转移酶的额外作用。