申请人长期从事炎症微环境诱导放射性脑损伤（RI）发病机制研究，成绩如下：①证明放射后Kv1.3及P2X7上调使小胶质细胞（MG）激活释放炎症介质形成炎症微环境诱导RI，揭示了放射后炎症微环境诱导RI的新机制（（NeuroOncol；Brain Behav Immun）；②证实放射后MG吞噬下降引起Nogo-A蓄积，最终导致微环境稳态失衡和白质修复障碍，为放射后MG改变微环境参与RI提供了新证据（Mol Neurobiol）；③改良RI治疗方案，在传统激素方案基础上联用自由基清除剂治疗RI患者，使治疗总有效率由35%提高至56%，为RI治疗开辟了新途径（J Neurooncol，Radiat Oncol）。发表SCI文章总数23篇，其中通讯20篇（共同通讯5篇，唯一通讯15篇），IF>5分7篇，总他引265次。获教育部新世纪优秀人才。拟开展炎症微环境与血管损伤在RI中的作用及机制研究。

My research interest focuses on radiation induced brain injury (RI). Main achievements are listed as follows. ① We proved that microglia (MG) were activated after radiation. Activated MG secreted proinflammatory factors which led to brain injury. Both Kv1.3 and P2X7 played important role in MG activation(NeuroOncol,Brain Behav Immun).② We proved that phagocytosis of MG was downregulated after radiation, leading to accumulation of myeline debrits and Nogo-A, which in turn caused the impairment of remyelination and axon regeneration（Mol Neurobiol）. ③We modified regimens for RI, which significantly improved therapeutic effect of RI（J Neurooncol，Radiat Oncol）. I have published 23 articles and reviews, 7 of which are with impact factor higher than 5. The number of citation for all papers is 265. The further project will be studying mechanisms of microvascular dysfunction and interaction between MG and pericytes in RI.