Crofford L J
Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0531, USA.
J Rheumatol Suppl. 1997 Jul;49:15-9.
It has been proposed that cyclooxygenase (COX)-1 and COX-2 subserve different physiologic functions largely because of the striking differences in their tissue expression and regulation. COX-1 displays the characteristics of a "housekeeping" gene and is constitutively expressed in almost all tissues. COX-1 appears to be responsible for the production of prostaglandins (PG) that are important for homeostatic functions, such as maintaining the integrity of the gastric mucosa, mediating normal platelet function, and regulating renal blood flow. In sharp contrast, COX-2 is the product of an "immediate-early" gene that is rapidly inducible and tightly regulated. Under basal conditions, COX-2 expression is highly restricted; however, COX-2 is dramatically upregulated during inflammation. For example, synovial tissues in patients with rheumatoid arthritis (RA) express increased levels of COX-2. In animal models of inflammatory arthritis, COX-2 increases in parallel with PG production and clinical inflammation. In vitro experiments have revealed increased COX-2 expression after stimulation with proinflammatory cytokines, such as interleukin 1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha), in many cell types, including synoviocytes, endothelial cells, chondrocytes, osteoblasts, and monocytes/macrophages. Another distinguishing characteristic of COX-2 is decreased expression in response to glucocorticoids. COX-2 is also increased in some types of human cancers, particularly colon cancer. Mechanisms underlying the association between COX-2 overexpression and tumorigenic potential may include resistance to apoptosis, or programmed cell death. Upregulated COX-2 expression undoubtedly plays a role in pathologic processes characterized by increased local PG production. One would predict, based on current information regarding the differential tissue expression of COX-1 and COX-2, that highly selective inhibitors of COX-2 will provide effective antiinflammatory activity with marked reduction in toxicity.
有人提出,环氧化酶(COX)-1和COX-2具有不同的生理功能,这主要是因为它们在组织表达和调控方面存在显著差异。COX-1表现出“管家”基因的特征,在几乎所有组织中组成性表达。COX-1似乎负责产生对稳态功能重要的前列腺素(PG),如维持胃黏膜的完整性、介导正常血小板功能以及调节肾血流量。与之形成鲜明对比的是,COX-2是一个“即刻早期”基因的产物,可快速诱导且受到严格调控。在基础条件下,COX-2的表达受到高度限制;然而,在炎症过程中COX-2会显著上调。例如,类风湿关节炎(RA)患者的滑膜组织中COX-2表达水平升高。在炎症性关节炎的动物模型中,COX-2与PG产生及临床炎症平行增加。体外实验表明,在许多细胞类型中,包括滑膜细胞、内皮细胞、软骨细胞、成骨细胞和单核细胞/巨噬细胞,用促炎细胞因子如白细胞介素1(IL-1)和肿瘤坏死因子-α(TNF-α)刺激后,COX-2表达增加。COX-2的另一个显著特征是对糖皮质激素反应时表达降低。在某些类型的人类癌症中,尤其是结肠癌,COX-2也会增加。COX-2过表达与致瘤潜能之间关联的潜在机制可能包括对细胞凋亡或程序性细胞死亡的抵抗。COX-2表达上调无疑在以局部PG产生增加为特征的病理过程中起作用。基于目前关于COX-1和COX-2组织差异表达的信息,可以预测,COX-2的高度选择性抑制剂将提供有效的抗炎活性,同时毒性显著降低。