辐射损伤的防治不仅有利于癌症放射治疗的顺利进行，而且对于应对核辐射事故具有现实意义。β-Catenin信号通路与损伤修复和组织再生等关系非常密切，但其在辐射损伤中的作用及调控机制仍未完全阐明。我们前期研究发现过氧化物酶PRDX6可减轻正常细胞受到的辐射损伤；PRDX6能与Wnt3a相互作用，并能激活下游β-Catenin信号通路。因而我们提出科学假设：PRDX6与Wnt3a结合后稳定了Wnt3a，促进后者与受体的结合进而激活β-Catenin信号通路，影响辐射后细胞和个体的损伤修复。本项目拟在前期工作基础上验证这一假设：阐明PRDX6与Wnt3a相互作用位点及对β-Catenin的激活机制，进一步揭示PRDX6/Wnt3a复合物对正常细胞和动物个体辐射损伤的影响和机制。本研究有望揭示β-Catenin信号通路在辐射损伤中的作用及PRDX6对其的调控机制，也为辐射的治疗提供新的思路与途径。

The prevention and treatment for radiation-induced injury is not only conducive to cancer radiotherapy, but also has practical significance to deal with nuclear accidents. β-Catenin signaling pathway is closed related to tissue repair and regeneration upon injuries, however, its role and regulatory mechanism in radiation-induced injury have not been fully elucidated. In our preliminary study, we found that peroxidase PRDX6 could alleviate radiation-induced injury of normal cells. Moreover, we also found that PRDX6 can interact with Wnt3a and activate β-Catenin signaling pathway. We therefore hypothesize that binding of PRDX6 and Wnt3a stabilizes Wnt3a, which promotes constitutive activation of the β-Catenin signaling pathway and contributes to tissue repair and regeneration after radiation. In this project, we will confirm the above hypothesis: elucidating the mechanism how PRDX6 activates β-Catenin by interaction with Wnt3a. Furthermore, we will also analyze the radio-protective role of PRDX6/Wnt3a complex for mice and human normal cells. This study is expected to reveal the role of β-signaling pathway in radiation injury and its regulatory mechanism by PRDX6/Wnt3a complex, which is likely to provide a new approach for the treatment of radiation-induced injury.