Hurst J S, Slater T F, Lang J, Juergens G, Zollner H, Esterbauer H
Chem Biol Interact. 1987 Feb;61(2):109-24. doi: 10.1016/0009-2797(87)90033-0.
The stimulation by ADP or arachidonic acid of the aggregation of human platelets in plasma was inhibited by 4-hydroxynonenal (HNE). This reduction of aggregation was time related, and was increased by prolonged preincubation of the platelets with the aldehyde. HNE was more potent than its homologue 4-hydroxypentenal (HPE). HNE was less active in decreasing the aggregation induced by calcium ionophore A23187 or collagen in comparison with ADP. HNE was inactive against aggregation of platelet-rich plasma (PRP) stimulated by thrombin whereas it potently inhibited the aggregation of washed platelets in response to both thrombin and collagen. Platelets were found to degrade HNE, and mechanisms additional to covalent binding to glutathione are indicated by the results obtained. The aldehydes, including HNE, generated by platelets originated principally from arachidonic acid metabolism.
4-羟基壬烯醛（HNE）可抑制血浆中ADP或花生四烯酸对人血小板聚集的刺激作用。这种聚集的减少与时间相关，并且通过使血小板与醛长时间预孵育而增强。HNE比其同系物4-羟基戊烯醛（HPE）更有效。与ADP相比，HNE在降低钙离子载体A23187或胶原诱导的聚集方面活性较低。HNE对凝血酶刺激的富血小板血浆（PRP）聚集无活性，而它能有效抑制洗涤血小板对凝血酶和胶原的聚集反应。发现血小板可降解HNE，所得结果表明除了与谷胱甘肽共价结合外还有其他机制。包括HNE在内的血小板产生的醛主要源自花生四烯酸代谢。
