目前，放射性肠组织损伤的治疗仍是个难题，研发放射性肠损伤的治疗新策略尤为迫切。我们实验室前期研究发现一个新型小分子化合物Me6，它能动员及募集骨髓中的内皮祖细胞至缺血组织，促进缺血下肢毛细血管新生。因此，我们推测Me6有可能通过调控骨髓内皮祖细胞的行为来促进辐射损伤肠组织的修复。我们拟选用致死剂量射线照射的小鼠模型，评估Me6是否具有促进辐射损伤肠组织修复的能力；利用骨髓GFP+细胞嵌合的小鼠模型，弄清Me6是否通过募集骨髓中的内皮祖细胞来发挥辐射损伤治疗作用；利用原代细胞（内皮祖细胞、小肠隐窝细胞）的辐照后克隆培养实验等分析Me6直接作用的靶细胞；进一步通过体外、体内实验阐明其发挥作用的信号通路和作用靶点，明确Me6发挥肠辐射损伤治疗作用的分子机制。本项目提出了化合物可以通过调控干细胞的行为来发挥肠辐射损伤治疗作用的新思路，研究结果将为我们今后开发出治疗肠辐射损伤的新型药物奠定基础。

To date, there are no effective pharmacological interventions to prevent the development of intestinal radiation injury. The work should be continued to find new therapeutic strategies for intestinal radiation injury. We previously found a novel small molecule, Me6, could increase the recruitment and incorporation of bone marrow endothelial progenitor cells (BM EPCs) into the ischemic limb and promoted functional angiogenesis. Thus, we postulate that Me6 might promote the repair and regeneration of intestinal radiation injury via the recruitment of endothelial progenitor cells. We plan to use the lethally-irradiated mice to evaluate the effect of Me6 on the repair of damaged intestine. By using BM GFP+ cells-reconstructed mice with lethally-irradation, we will further evaluate whether Me6 recruit BM EPCs into damaged intestine and promote the regeneration of intestine epithelial cells. In combination with in vitro and in vivo experiments, we will investigate the direct target cells of Me6, the downstream signal pathway and the target genes. Our goal is to reveal the role of Me6 on the repair and regeneration of intestinal tissue and understand the regulation mechanism of Me6. The project will provide a novel strategy to find a therapeutic molecule via regulation of stem/progenitor cells.