Inhibition of Thromboxane Formation as the Antiplatelet Mechanism of 3,4-Dihydroxyxanthone and Quercetin Pentaacetate

3,4-Dihydroxyxanthone 和 Quercetin Pentaacetate 兩種抗血小板藥物之作用機轉在於抑制血栓素的形成

林獻誠(Hsien-Cheng Lin) ； 劉宏文(Hong-Wen Liu) ； 林忠男(Chun-Nan Lin) ； 鄧哲明(Che-Ming Teng)

《The Kaohsiung Journal of Medical Sciences》 7卷10期 (1991/10) Pp. 505-512

https://doi.org/10.6452/KJMS.199110.0505

摘要

合成化合物3,4-dihydroxyxanthone和由天然物quercetin經乙稀化形成之quercetin pentaacetate可抑制花生四烯酸與膠原所造成之血小板凝集與ATP之放，但對血小板活化因子（PAF）所引起之上述反應無影響，此抑制作用為可逆性，且與所用之濃度有關，而由花生四烯酸與膠原引起洗滌兔子血小板之血栓素B2形成，可被此兩種抗血小格藥物抑制；3,4-dihydroxyxanthon和quercetin pentaacetate 可抑制人類富含血小板血漿因受ADP及腎上腺素所引發之凝集反應之第二相，而對第一相則無影響，而在全血中兩種抗血小板藥物也可抑制由花四烯酸與膠原所引起之血小板凝集反應，且也與所用之濃度有關。總結以上結果顯示，3,4-dihydroxyxanthon與quercetin pentaacetate 二者之抗血小板作用是起因於抑制血栓素之形成而來。

並列摘要

3,4-Dihydroxyxanthone and quercetin pentaacetate were shown to inhibit the aggregation and ATP release of washed rabbit platelets induced by collagen and arachidonic acid, but were not induced by PAF. This inhibition was reversible and in a concentration-dependent manner. The thromboxane B2 formatio of washed rabbit platelets, which was caused by arachidonic acid and collagen, was also suppressed by both antiplatelet agents. In human platelet-rich plasma, 3,4-dihydroxyxanthon and quercetin pentaacetate inhibited the secondary, but not the primary aggregation induced by ADP and epinephrine. Both antiplatelet agents also inhibited collagen- and arachidonic acid-induced aggregation in whole blood in a dose-dependent manner. It is concluded that the antiplatelet effects of 3,4-dihydroxyxanthon and quercetin pentaacetate are due to the inhibition of thromboxane formation.

並列關鍵字

3,4-dihydroxyxanthone ； quercetin pentaacetate ； thromboxane formation