与以往对活性氧（ROS）的认识不同，最近的研究工作显示出氧依赖的氧化还原系统是启动创伤修复级联反应中必不可缺的一环。我们在前期工作中发现人角质细胞损伤后可在短期内出现ROS、PGE2及ERK的明显升高，在这一发现基础上并结合文献，提出并以期证实NOX-1为创伤后ROS主要来源；ERK为创伤后连接NOX-1／ROS与COX-2／PGE2的重要信号通路；存在NOX-1／ROS－ERK-COX-2／PGE2信号通路，并作为启动早期炎症反应的信号途径对创伤修复具有重要调节作用的假设。该假设为原创性首次提出，该研究的完成不仅可完善创伤修复发生的分子生物学机制，而且可望将NOX-1作为干预的目标来提出新的治疗措施。

Different to historically views as purely harmful, recent evidences suggest that reactive oxygen species (ROS) play a critical role in initiating wound healing. Our preliminary study showed that ROS, ERK and PGE2 successively increased and have a closely correlation after keratinocyte damage. We hypothesize that NOX-1 is a main enzymatic source of ROS generation after keratinocyte damage and there is a NOX-1／ROS－ERK－COX-2／PGE2 signal pathway, serve as a critical regulator for early inflammatory response of wound healing. In this study,we will testify the original hypothesis and explore the molecular mechanisms for wound healing.