Roles Of Cyclooxygenase-1 and -2 In UV-induced Skin Canc

流行病学研究表明，紫外线（UV）辐射导致皮肤损伤，是皮肤癌发展的主要环境因素。研究了COX-1和COX-2缺乏以及COX-1和COX-2选择性抑制剂在急性紫外线剂量诱导的皮肤损伤中的作用。结果表明，与野生型小鼠相比，缺乏COX-2而不缺乏COX-1的小鼠表现出剂量依赖性的表皮皮肤损伤和细胞死亡增加。与COX-1缺失或野生型小鼠相比，COX-2缺失小鼠的细胞凋亡水平增加了约2.5倍。前列腺素E2受体EP2和EP4已被证明参与COX-2对紫外线诱导的皮肤损伤的保护作用。此外，EP2和EP4激活的信号通路在UVB诱导的皮肤损伤保护中的作用已被部分阐明，并表明分别涉及PKA和Akt。

Epidemiological studies indicate that ultra violet (UV) radiation causes skin damage and is a major environmental agent in skin cancer development. The effects of COX-1 and COX-2 deficiency, as well as COX-1 and COX-2 selective inhibitors, in acute UV dose induced skin damage have been studied. The results indicate that mice deficient in COX-2, but not COX-1, exhibit dose dependent increases in epidermal skin damage and cell death compared to wild type mice. Levels of apoptosis were increased about 2.5 -fold in COX-2 null mice compared to COX-1 null or wild type mice. The prostaglandin E2 receptors, EP2 and EP4, have been demonstrated to be involved in COX-2's protective effect against UV induced skin damage. Furthermore, the signaling pathways activated by EP2 and EP4 in the protection of UVB induced skin damage have been partially elucidated, and shown to involve PKA and Akt, respectively.