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前列腺素E0抑制兔动脉壁中胶原蛋白和糖胺聚糖的合成。

PGE0 inhibits collagen and glycosaminoglycan-synthesis in the rabbit arterial wall.

作者信息

Rodrigues M, Sinzinger H, Kritz H, Peskar B A, O'Grady J, Rogatti W

机构信息

Department of Nuclear Medicine, University of Vienna, Austria.

出版信息

Vasa. 1995;24(4):333-6.

PMID:8533442
Abstract

The influence of 13,14-dihydro-PGE1 (PGE0), a biologically active metabolite of PGE1, on collagen and glycosaminoglycan synthesis by the rabbit arterial wall was assessed and compared with the effect of PGE1. Collagen (COL) and glycosaminoglycan (GAG) synthesis was measured using 14C proline- and 35S-incorporation respectively and both were subsequently quantified by autoradiography. PGE1 decreased GAG-synthesis by 40%, while PGE0 caused a 25% decrease. COL-synthesis after PGE1 treatment was diminished by 35%, while the biologically active metabolite caused a drop of 30%. Five and 15 micrograms/kg doses of both compounds were almost equally effective, 1 microgram was without effect. These findings indicate that PGE0 shares the inhibitory effect of PGE1 on COL and GAG biosynthesis. This metabolite has about 60 to 70% of the biological activity of its parent compound PGE1. These results suggest that part of the effects of PGE1 in inhibiting extracellular matrix production could be due to its metabolite PGE0.

摘要

评估了前列腺素E1(PGE1)的生物活性代谢产物13,14-二氢-PGE1(PGE0)对兔动脉壁胶原蛋白和糖胺聚糖合成的影响,并与PGE1的作用进行了比较。分别使用14C脯氨酸掺入法和35S掺入法测量胶原蛋白(COL)和糖胺聚糖(GAG)的合成,随后通过放射自显影对两者进行定量。PGE1使GAG合成减少40%,而PGE0导致减少25%。PGE1处理后COL合成减少35%,而这种生物活性代谢产物导致减少30%。两种化合物5微克/千克和15微克/千克的剂量效果几乎相同,1微克则无效果。这些发现表明,PGE0与PGE1一样具有对COL和GAG生物合成的抑制作用。这种代谢产物具有其母体化合物PGE1约60%至70%的生物活性。这些结果表明,PGE1抑制细胞外基质产生的部分作用可能归因于其代谢产物PGE0。

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