乏氧是肿瘤的特征，同时也影响放射导致的正常组织损伤。迄今对乏氧和放射性直肠纤维化的关系还不明确。我们前期研究证实照射后的组织乏氧促进放射性直肠纤维化发展。另外预实验提示，和乏氧相关的miRNA-210在放射性直肠晚期损伤组织中表达增加，但二者影响放射性纤维化的机制还有待了解。为此我们提出假设，放射后的组织乏氧和放射性直肠纤维化密切相关，且很可能受miRNA-210及其相关基因的调节。为验证这一假设，我们将通过体外细胞模型，放射性直肠纤维化小鼠模型，采用质粒转染，乏氧培养，ELISA等手段，从分子，细胞，组织及动物等多方面探讨照射后的组织乏氧对放射性直肠损伤的影响，明确miRNA-210及乏氧微环境与放射性直肠纤维化的相互关系。本研究将从放射引起的组织乏氧这个新视点为揭示放射性直肠纤维化发生机制奠定基础，进而为放射性直肠炎的防治提供新思路。

Hypoxia has been found well not only in solid tumors but also in radiation-induced normal tissue injury. However, the relation between hypoxia and radiation-induced rectal fibrosis is still unclear. Our previous studies have demonstrated radiation-induce tissue hypoxia contributed the development of rectal fibrosis, and microRNA-210 (miRNA-210) increased in murine rectum after radiation, which were demomstrated to be related with hypoxia-inducible factors family. These results suggested miRNA-210 and hypoxia maybe play a role in radiation-induced fibrosis. In this study, we will study the role of hypoxia in induction and development of fibrosis, and the relation of hypoxic signal and miRNA-210 in vitro and in vivo by hypoxic culture, miRNA-210 transfection, ELISA, mice model of radiation-induced rectal fibrosis and so on. Our study may be good to know the radiation-induced rectal fibrosis well and to improve the quality of life of patients who received pelvic radiotherapy.