Bioactive Amide of Prostaglandin E₁ and Ethanolamine Plasmalogen Analog of Platelet-Activating Factor Inhibits Several Pathways of Human Platelet Aggregation

V. I. Kulikov^* and G. I. Muzya

Research and Development Center for Medical Biotechnology, Ministry of Public Health of the Russian Federation, ul. Shchukinskaya 6, Moscow, 123182 Russia; fax: (095) 190-0100

^* To whom correspondence should be addressed.

Received September 15, 1999; Revision received November 9, 1999

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The influence of an amide of prostaglandin E₁ and ethanolamine plasmalogen platelet-activating factor analog 1-O-alk-1´-enyl-2-acetyl-sn-glycero-3-phospho-(N-11alpha,15alpha-dioxy-9-keto-13-prostenoyl)ethanolamine (PGE₁-PPAF) on platelet-activating factor (PAF)-, ADP-, and thrombin-induced human platelet aggregation has been studied. It was found that PGE₁-PPAF inhibits the PAF-, ADP-, and thrombin-induced platelet aggregation in platelet-rich plasma. 1-O-alk-1´-enyl-2-acetyl-sn-glycero-3-phosphoethanolamine inhibited PAF-induced aggregation up to 50% but had no influence on platelet aggregation induced by ADP or thrombin. The ethanolamine plasmalogen analog of PAF 1-O-alk-1´-enyl-2-acetyl-sn-glycero-3-phospho-(N-palmitoyl)ethanolamine, having a palmitoyl residue instead of PGE₁, did not inhibit platelet aggregation induced by PAF, ADP, or thrombin. We propose that inhibition of human platelet aggregation by PGE₁-PPAF is mediated by its action on platelet PAF-receptors and the adenylate cyclase system.

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KEY WORDS: platelet-activating factor, amide of prostaglandin E₁ and a PAF analog, prostaglandin E₁, platelets

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