缺血引发的炎症反应是许多疾病共有的病理机制，除超早期恢复血供外无理想的治疗方法，亟待寻求新的药物靶标及筛选体系。炎性细胞浸润是加重炎症反应的最重要的机制之一，如能阻断炎性细胞向病灶迁移，将为治疗缺血性损伤提供新的思路。CKLF1是由我国科学家首次发现的新趋化因子，特异性的在缺血性损伤中表达增加，拮抗其活性可缓解缺血性损伤，具备成为药物靶点的潜能，且用我们构建的以CKLF1为靶点的药物筛选体系获得的新型化合物IMM-H004，具有较好的改善缺血性损伤的作用。但CKLF1作为新靶点尚需完成以下系统性药理学研究：①揭明CKLF1及其受体介导细胞迁移的生物学基础；②构建以细胞迁移为检测目标的药物筛选体系；③采用分子对接等方法揭明候选化合物与CKLF1的分子结合位点。本项目的实施将对我国首次在国际上提出新型药物治疗靶点，提升我国科技水平，以及发展具有中国特色的原创药物具有重大的理论意义和应用价值。

The inflammation induced by ischemia is a common pathological mechanism in many diseases. There is no ideal therapeutic method except for restoring the blood supply in the early stage. Therefore, new drug targets and screening systems are urgently needed. Inflammatory cell infiltration is one of the most important mechanisms to aggravate the inflammation. It will pave a new way for the treatment of ischemic injury if the migration of inflammatory cells to the lesion is blocked. CKLF1, a new chemokine first discovered by Chinese scientists, was specificly increased in the ischemic injury. And the ischemic injury was relieved by antagonizing the activity of CKLF1. Therefore, CKLF1 is a potential drug target. Moreover, the new compound IMM-H004 which was screened from our constructed screening system based on CKLF1 relieved the ischemic injury. However, as a new target there still need to reveal something about CKLF1 as followed: the biological basis of cell migration mediated by CKLF1 and its receptor; the construction of screening system for drug target detection based on cell migration; the binding sites of CKLF1 and candidate compounds using molecular docking method. The implementation of this project will be the first time to put forward the new drug target by our country in the world. This has great theoretical significance and application value in improving the level of science and technology, and developing the original drug.