...
首页> 外文期刊>Medical science monitor : >COX-2 inhibitors and metabolism of essential fatty acids.
【24h】

COX-2 inhibitors and metabolism of essential fatty acids.

机译:COX-2抑制剂和必需脂肪酸的代谢。

获取原文
           

摘要

Selective COX-2 inhibitors increase the risk of myocardial infarction andstroke that is attributed to their ability to inhibit prostacyclin (PGI(2)), lipoxins, resolvins, andendothelial nitric oxide (eNO) but not platelet COX-1 derived thromboxane A(2) (TXA(2)). In contrast,aspirin blocks both COX-1 and COX-2 enzymes that, in turn, increases intracellular concentrations ofdihomo-gamma-linolenic acid (DGLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoicacid (DHA) and reduced formation of eicosanoids. On the other hand, such an increase is much less withspecific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway.DGLA, AA and EPA form precursors to PGE(1) , PGI(2), and PGI(3) respectively, which are potent vasodilatorsand platelet anti-aggregators, and thus aid in the prevention of thrombus formation. EPA has anti-arrhythmicaction, and EPA, DHA (docosahexaenoic acid), DGLA, and PGE(1) have anti-inflammatory actions as well.EPA, DHA, and AA augment eNO formation that has anti-atherosclerotic action. Hence, combining EFAs withCOX-2 inhibitors will prevent thrombotic cardiovascular events.
机译:选择性COX-2抑制剂会增加心肌梗塞和中风的风险,这归因于其抑制前列环素(PGI(2)),脂类毒素,分辨蛋白和内皮型一氧化氮(eNO)的能力,但不能抑制血小板产生于COX-1的血栓烷A(2)。 (TXA(2))。相反,阿司匹林同时阻断COX-1和COX-2酶,从而增加细胞内二高-γ-亚麻酸(DGLA),花生四烯酸(AA),二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)的细胞内浓度并降低类花生酸的形成。另一方面,特异性COX-2抑制剂的这种增加要少得多,因为它们不会通过COX-1途径阻止类花生酸的形成.DGLA,AA和EPA是PGE(1),PGI(2)和PGI(3)分别是有效的血管扩张剂和血小板抗聚集剂,因此有助于预防血栓形成。 EPA具有抗心律失常作用,而EPA,DHA(二十二碳六烯酸),DGLA和PGE(1)也具有抗炎作用.EPA,DHA和AA增强了具有抗动脉粥样硬化作用的eNO的形成。因此,将EFA与COX-2抑制剂联合使用可预防血栓性心血管事件。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号