摘要
景:腹主动脉瘤(AAA)是西方国家的主要死亡原因之一,目前外科手术仍是唯一的治疗方法,但死亡率和费用都很高。许多药物正在研究以减少生长和防止AAA破裂,这些药物针对不同的病理途径,尤其是环氧合酶(COX)过度产生脯氨酸类药物,动脉瘤内血栓起着不利的作用。在AAA的进展中起关键作用,血小板是血栓素A2等前列腺素的主要来源。 目的:本文对心血管疾病中脯氨酸的产生和下游途径的研究,尤其是在AAA方面的研究进行了综述。 结果与结论:COX抑制剂或前列腺素受体拮抗剂在AAA动物模型中均有不同程度的研究,但在人AAA中,以乙酰水杨酸(阿司匹林,ASA)为主要抑制剂的抗血小板治疗研究较少,最后,我们报告了接受血栓素2抑制剂BM-573抑制动脉瘤生长的AAA模型的初步结果。
关键词: 腹主动脉瘤、前列腺素、血栓素A2、乙酰水杨酸、血小板、环氧合酶。
图形摘要
Current Drug Targets
Title:Therapeutic Applications of Prostaglandins and Thromboxane A2 Inhibitors in Abdominal Aortic Aneurysms
Volume: 19 Issue: 11
关键词: 腹主动脉瘤、前列腺素、血栓素A2、乙酰水杨酸、血小板、环氧合酶。
摘要: Background: Abdominal aortic aneurysm (AAA) is one of the leading causes of death in western countries. Surgery is still, at the present time, the sole treatment that has however a significant mortality and cost rate. Many pharmacological agents are under investigation aiming to reduce growth and prevent AAA rupture. These drugs target different pathological pathways and, notably, the excessive production of prostanoids by cyclooxygenases (COX). Intra-aneurysmal thrombus plays an adverse key role in the progression of AAA, platelets being a primary source of prostanoids as thromboxane A2.
Objective: In this review, we summarize studies targeting prostanoids production and down-stream pathways in cardiovascular diseases, and more specifically in AAA.
Results and Conclusion: Various inhibitors of COX or antagonists of prostanoids receptors have been investigated in AAA animal models with conflicting results. In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor. Finally, we report preliminary promising results of a model of AAA in rats receiving a thromboxane A2 inhibitor, BM-573 that induced a reduction of aneurysmal growth.
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Cite this article as:
Therapeutic Applications of Prostaglandins and Thromboxane A2 Inhibitors in Abdominal Aortic Aneurysms, Current Drug Targets 2018; 19 (11) . https://dx.doi.org/10.2174/1389450119666171227224314
DOI https://dx.doi.org/10.2174/1389450119666171227224314 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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