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非甾体抗炎药(nonsteroidal anti-inflammatory drugs,NSAIDs)通过抑制前列腺素合成中的环氧化酶(cyclooxygenase,COX)、从而阻断花生四烯酸生成前列腺素,发挥镇痛抗炎的作用。但因其胃肠道、肾功能、心血管和血小板等方面的副作用, 限制了它的广泛使用。COX存在两种同分异构体,其中环氧化酶-2(COX-2)主要在损伤或炎症部位表达,并合成前列腺素类物质,由此推动了选择性COX-2抑制剂的研制。普遍认为它与传统的NSAIDs的镇痛抗炎性能相当,但副作用减少。目前,这种学说得到了广泛的认同,然而,COX-2抑制剂的应用还有待深入认识。
Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their analgesic and anti-inflammatory effects by inhibiting cyclooxygenase (COX) in prostaglandin synthesis and thereby blocking the production of prostaglandins by arachidonic acid . However, its widespread use has been limited by the side effects of gastrointestinal tract, renal function, cardiovascular and platelet. There are two isoforms of COX, in which cyclooxygenase-2 (COX-2) is predominantly expressed at the site of injury or inflammation and synthesizes prostaglandins, thereby promoting the development of selective COX-2 inhibitors . It is generally believed that it has comparable analgesic and anti-inflammatory properties to traditional NSAIDs but with fewer side effects. At present, this theory has been widely recognized, however, the application of COX-2 inhibitors remains to be fully understood.