抑郁症是严重危害人类健康的精神疾病，氧化应激与炎症反应在抑郁症中发挥着重要作用，但其关键作用分子及调节机制尚不明确。我们前期临床及动物研究一致表明，乙二醛酶1（Glyoxalase I，Glo1）在抑郁组中显著低表达，而Glo1作为氧化应激通路的重要调节分子，可能通过调控NLRP3/Caspase-1炎性小体的激活参与抑郁症的病理过程。据此，本课题拟开展以下工作：1）在抑郁患者及动物模型中明确Glo1与抑郁症的关系；2）在抑郁模型中探讨Glo1与氧化应激及NLRP3/Caspase-1炎性小体通路相关性；3）在星形胶质细胞中明确Glo1负调控ROS/NLRP3/Caspase-1信号通路介导的炎症反应；4）在动物模型和细胞模型中验证Glo1的保护作用。本研究旨在进一步明确Glo1在抑郁症发病机制中的作用，为寻找新的药物治疗靶标奠定理论基础。

Depression is a mental illness that seriously endangers human health. Oxidative stress and inflammation play an important role in the pathogenesis of depression. However, the key molecular mechanisms of oxidative stress and inflammation in depression are still unclear. Our previous clinical and animal studies have consistently revealed that glyoxalase I (Glo1) was significantly down-regulated in the depressed group. As an important regulator of oxidative stress pathway, Glo1 may participate in the pathological process of depression by regulating the activation of NLRP3/caspase-1 inflammasome. Accordingly, we carry out the following researches. 1) To clarify the correlation between Glo1 and depression in patients and animal models; 2) To explore the correlation among Glo1, oxidative stress and the pathway of NLRP3/Caspase-1 inflammasome in depression models; 3) To clarify whether Glo1 negatively regulates ROS/NLRP3/Caspase-1 mediated inflammatory response pathway in astrocytes; 4) And finally to verify the protective effect of Glo1 in animal models and astrocyte models. This study aims to elucidate the role of Glo1 in the pathogenesis of depression, and lay a theoretical foundation for finding new drug targets.