早期预防并降低海马神经元放射性损伤是提高患者生活质量的重要手段。我们预实验发现丹参酮IIA通过激活转录因子Nrf2调节糖酵解酶ALDOC的改变，进而调控糖酵解并诱导自噬从而减轻海马神经元放射性损伤。据此我们推测：丹参酮IIA能通过Nrf2/ALDOC调节糖酵解及自噬从而减轻海马神经元放射性损伤。本项目将首先通过体内外实验验证丹参酮IIA具有减轻放射性神经损伤的生物学功能；然后利用生物芯片、生物信息学预测等技术探讨丹参酮IIA通过Nrf2引起ALDOC的改变，以及进一步诱导糖酵解及自噬，从而调节放射性损伤的分子机制；最后通过转基因动物验证ALDOC在丹参酮IIA对海马放射性损伤保护中的作用。本项目完成可望为丹参酮IIA对海马放射性损伤保护提供新的理论及临床试验依据。

Early prevention and reduction of radiation injury of hippocampal neurons is an important means to improve the life quality of patients. We have found that tanshinone IIA can regulate the expression of ALDOC, which regulates glycolysis and induces autophagy promote hippocampal neurons to survive after radiation injury, by upregulating transcription factor Nrf2. Therefore, we proposed: tanshinone IIA protects hippocampal neurons from radiation injury via Nrf2/ALDOC induced glycolysis and autophagy. In this project, firstly, the biological function of tanshinone IIA will be verified by in vitro and in vivo experiments. Secondly, the molecular mechanism of Nrf2/ALDOC induced by tanshinone IIA and the further induction of glycolysis and autophagy will be studied using bio-chip, bioinformatic prediction and other techniques. Finally, transgenic animals will be used to verify the effect of ALDOC on the protective effects of tanshinone IIA on hippocampus radiation injury. From this project, it is expected to provide a new theoretical basis for the protection of radiation injury by tanshinone IIA and provide the basis for the follow-up clinical trials.