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首页> 外文期刊>Circulation: An Official Journal of the American Heart Association >Cardiovascular Consequences of Prostanoid I Receptor Deletion in Microsomal Prostaglandin E Synthase-1-Deficient Hyperlipidemic Mice
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Cardiovascular Consequences of Prostanoid I Receptor Deletion in Microsomal Prostaglandin E Synthase-1-Deficient Hyperlipidemic Mice

机译:微粒体前列腺素E合酶-1缺乏症的高脂血症小鼠的前列腺素I受体删除的心血管后果。

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摘要

BACKGROUND: Inhibitors of cyclooxygenase-2 alleviate pain and reduce fever and inflammation by suppressing the biosynthesis of prostacyclin (PGI(2)) and prostaglandin E-2. However, suppression of these prostaglandins, particularly PGI(2), by cyclooxygenase-2 inhibition or deletion of its I prostanoid receptor also predisposes to accelerated atherogenesis and thrombosis in mice. By contrast, deletion of microsomal prostaglandin E synthase 1 (mPGES-1) confers analgesia, attenuates atherogenesis, and fails to accelerate thrombogenesis, while suppressing prostaglandin E-2, but increasing biosynthesis of PGI(2).
机译:背景:环氧合酶2抑制剂通过抑制前列环素(PGI(2))和前列腺素E-2的生物合成来减轻疼痛并减少发烧和炎症。但是,通过环加氧酶-2抑制或删除其前列腺素I抑制这些前列腺素,尤其是PGI(2),也有加速小鼠动脉粥样硬化和血栓形成的倾向。相比之下,微粒体前列腺素E合酶1(mPGES-1)的缺失赋予镇痛作用,减弱动脉粥样硬化的发生,并不能加速血栓形成,同时抑制前列腺素E-2,但增加了PGI(2)的生物合成。

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