Gustafson-Svärd C, Lilja I, Hallböök O, Sjödahl R
Clinical Research Centre, Department of Biomedicine and Natural Sciences, The Baltic International School of Public Health (BIH), Karlskrona, Sweden.
Ann Med. 1997 Jun;29(3):247-52. doi: 10.3109/07853899708999342.
Epidemiological and experimental studies indicate an inverse relationship between the risk of colon cancer development and intake of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). All NSAIDs are known inhibitors of cyclo-oxygenase, the enzyme responsible for converting arachidonic acid to prostaglandins. Prostaglandins have been implicated in the pathogenesis of colon cancer and it has been suggested that the preventive effect of NSAIDs is due to inhibition of cyclo-oxygenase activity. Cyclo-oxygenase exists in two different isoforms, cyclo-oxygenase-1 and cyclo-oxygenase-2, and data obtained during the last few years have suggested that cyclo-oxygenase-2 might be involved in both human and experimental colon carcinogenesis. The purpose of this review is to provide an update on recent studies regarding cyclo-oxygenase, in particular cyclo-oxygenase-2, in relation to colon cancer in humans and in experimental models.
流行病学和实验研究表明，结肠癌发生风险与阿司匹林及其他非甾体抗炎药（NSAIDs）的摄入量之间存在负相关关系。所有NSAIDs都是已知的环氧化酶抑制剂，环氧化酶负责将花生四烯酸转化为前列腺素。前列腺素与结肠癌的发病机制有关，有人认为NSAIDs的预防作用是由于其对环氧化酶活性的抑制。环氧化酶以两种不同的同工型存在，即环氧化酶-1和环氧化酶-2，过去几年获得的数据表明，环氧化酶-2可能参与人类和实验性结肠癌的发生。这篇综述的目的是提供关于环氧化酶，特别是环氧化酶-2，在人类和实验模型中与结肠癌相关的最新研究情况。
