作业帮求阿司匹林的英文药理作用，带中文翻译 字数多一点
来源：学生作业帮 编辑：作业帮 分类：综合作业 时间：2024/05/18 10:53:00
求阿司匹林的英文药理作用，带中文翻译 字数多一点
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本品具有镇痛、解热，抗炎、抗风湿及抗血栓作用。 本品及所有的非甾体抗炎药（NSAID)的镇痛作用主要是外周性，它降低局部因缓激肽组胺等介质引起的疼痛的敏感性，有别于麻醉药的中枢性抑制镇痛作用。 镇痛消肿作用机制在于抑制花生四烯酸的代谢。花生四烯酸是细胞膜磷脂的成分之一，是由致炎症因子活化磷脂酶后形成，再经环氧酶（cyclooxygenase，COX)的代谢作用而合成一系列的代谢产物，包括多种前列腺素（PG)，如PGG2、PGH2、PGI2、PGE1、PGE2和血栓素。前列腺素是很强的炎症介质，引起局部组织的疼痛、充血、水肿和破坏。花生四烯酸的另一代谢途径为由脂氧酶而合成白三烯和HPETE。阿司匹林通过对COX结构中的丝氨酸的乙酰化而抑制COX，使前列腺素减少。阿司匹林和大部分的NSAID一样对脂氧酶的作用并不明显。在高浓度时，阿司匹林有清除促进炎症和组织破坏的超氧化物、羟基和其他自由基的作用。阿司匹林对生理型COX（COX-1)抑制较强，因此也可抑制胃、肾组织内生理性前列腺素合成，使胃酸产生过多，胃粘液生成减少，食道胃肌张力松弛，临床出现胃消化不良，甚至胃溃疡。在某些条件下，肾血流量减少，引起可逆性肾功能不全。它抑制子宫痉挛性收缩。 阿司匹林的解热作用是因下丘脑（体温中枢)的前列腺素合成受抑所致。本品也可因影响COX而抑制血小板中血栓素（TXA2)的合成以致降低血小板聚集。
This product has analgesic, antipyretic, anti-inflammatory, anti-rheumatic and anti-thrombotic effect. The analgesic effect of the goods and all of the non-steroidal anti-inflammatory drugs (NSAID) is a peripheral, it reduces the partial sensitivity to pain caused by bradykinin such as histamine medium, central inhibition Unlike anesthetics analgesic effect. The analgesic swelling mechanism of action is inhibition of arachidonic acid metabolism. Arachidonic acid is one of the components of the membrane phospholipids, is formed after activation of phospholipase by induced by inflammatory factors, then the metabolic effects of cyclooxygenase (cyclooxygenase, COX) synthesized a series of metabolites, including a variety of prostaglandin (PG), such as PGG2, PGH2, PGI2, PGE1, PGE2, and thromboxane. Prostaglandins are highly inflammatory mediators, causing local tissue pain, congestion, edema, and destruction. The other metabolic pathways of arachidonic acid by the lipoxygenase and synthesis of leukotrienes and HPETE. Inhibition by aspirin by acetylation of the serine of the structure of COX while COX, so that the decrease in prostaglandin. Aspirin and most of the NSAID role of lipoxygenase is not obvious.At high concentrations, aspirin has cleared promote inflammation and tissue destruction of superoxide, hydroxyl and other radicals. Aspirin inhibit strong physiological type COX (COX-1), and therefore also inhibit the physiological synthesis of prostaglandins in the stomach, kidney tissue, to make gastric acid production too much, decreased production of gastric mucus, the esophagus stomach muscle tension and relaxation, clinical gastric digestion poor or gastric ulcer. Under certain conditions, the decrease in renal blood flow, cause reversible renal insufficiency. It inhibits the spasmodic contraction of the uterus. Antipyretic effect of aspirin is due to the hypothalamus (body Wenzhong Shu) prostaglandin synthesis inhibition. This product can also be due to the impact of COX inhibition of platelet thromboxane (TXA2) synthesis so as to reduce platelet aggregation.
This product has analgesic, antipyretic, anti-inflammatory, anti-rheumatic and anti-thrombotic effect. The analgesic effect of the goods and all of the non-steroidal anti-inflammatory drugs (NSAID) is a peripheral, it reduces the partial sensitivity to pain caused by bradykinin such as histamine medium, central inhibition Unlike anesthetics analgesic effect. The analgesic swelling mechanism of action is inhibition of arachidonic acid metabolism. Arachidonic acid is one of the components of the membrane phospholipids, is formed after activation of phospholipase by induced by inflammatory factors, then the metabolic effects of cyclooxygenase (cyclooxygenase, COX) synthesized a series of metabolites, including a variety of prostaglandin (PG), such as PGG2, PGH2, PGI2, PGE1, PGE2, and thromboxane. Prostaglandins are highly inflammatory mediators, causing local tissue pain, congestion, edema, and destruction. The other metabolic pathways of arachidonic acid by the lipoxygenase and synthesis of leukotrienes and HPETE. Inhibition by aspirin by acetylation of the serine of the structure of COX while COX, so that the decrease in prostaglandin. Aspirin and most of the NSAID role of lipoxygenase is not obvious.At high concentrations, aspirin has cleared promote inflammation and tissue destruction of superoxide, hydroxyl and other radicals. Aspirin inhibit strong physiological type COX (COX-1), and therefore also inhibit the physiological synthesis of prostaglandins in the stomach, kidney tissue, to make gastric acid production too much, decreased production of gastric mucus, the esophagus stomach muscle tension and relaxation, clinical gastric digestion poor or gastric ulcer. Under certain conditions, the decrease in renal blood flow, cause reversible renal insufficiency. It inhibits the spasmodic contraction of the uterus. Antipyretic effect of aspirin is due to the hypothalamus (body Wenzhong Shu) prostaglandin synthesis inhibition. This product can also be due to the impact of COX inhibition of platelet thromboxane (TXA2) synthesis so as to reduce platelet aggregation.