慢性脑低灌注（CCH）与多种缺血性脑血管疾病的病理发生密切相关，临床上尚缺乏有效的干预措施。我们前期研究显示：过度自噬在CCH导致的神经细胞死亡及认知功能障碍的过程中发挥了一定的作用，此外，CCH大鼠模型存在肠道菌群异常，改善肠道菌群稳态可降低自噬体数量及神经炎症因子表达。因此，我们认为肠道菌群变化和神经自噬损伤之间可能存在着千丝万缕的联系，但具体作用及作用机制尚不明确。本项目拟采用16s rRNA测序技术分析CCH大鼠肠道菌群的精细特征差异；通过液相色谱-质谱联用技术和磁共振波谱技术分析肠道代谢产物及神经代谢产物的变化，探索两者之间的关联性；利用神经组织学、神经行为学及分子生物学技术明确肠道菌群改变对CCH神经自噬损伤影响的关键环节及调控机制，为肠道微生物-神经系统相互作用提供新的理论依据，为改善慢性缺血性神经损伤提供新的干预途径。

Chronic cerebral hypoperfusion (CCH) is associated with several ischemic cerebrovascular diseases.However,there is still lack of effective clinical treatment. Our team found the excessive autophagy induced by CCH may contribute to the process of neuronal death and cognitive impairment. Furthermore,the rat model of CCH had abnormal gut microorganisms.In addition,improvement of intestinal flora homeostasis can reduce the number of autophages and the expression of neuroinflammatory factors. Hence,we believe there may be a relationship between the gut microorganisms and autophagic damage of neuronal cells.However, the role and mechanism of gut microorganisms on nuoronal autophagic damage are still unclear.In this study, 16s rRNA sequencing is used to analyze subtle features of intestinal microorganisms of CCH rats；High performance liquid chromatography-mass spectrometry and magnetic resonance spectroscopy are used to analyze the changes of intestinal metabolites and neurometabolites; The correlation between intestinal metabolites and neurometabolites is further explored; Neurohistology, neurobehaviology and molecular biology are used to clarify the role and mechanism of gut microorganisms on neuronal autophagic damage. This study might provide new evidence for the interaction between gut microorganisms and nervous system as well as a novel strategy for the repair of ischemic neuronal injury.