抑郁症是一种全球性公共健康问题，但由于发病机制复杂，涉及系统众多，抗抑郁药物研究虽是全球热点但进展缓慢。近年来，线粒体功能障碍导致的能量代谢水平低下以及突触可塑性受损等在抑郁症的发病机制中日益受到重视，有望成为新的研究靶点。我们在前期研究中观察到黄芩及其活性成分黄芩苷具有良好的抗抑郁作用，但其机理仍不清楚。结合相关文献报道，黄芩苷可上调沉默信息调节因子（SIRT）1发挥线粒体保护作用，我们推测黄芩苷的抗抑郁机制可能与此有关。本项目拟采取慢性不可预知性温和刺激动物抑郁模型，以线粒体能量代谢为核心，围绕其对神经元功能的调节，以及AMP依赖的蛋白激酶（AMPK）/SIRT1对线粒体功能的调节来探讨黄芩苷的抗抑郁机制，期望为抗抑郁新药的研发提供新的角度和依据。

Depression is a global public health problem. Due to the complexity of the pathogenesis of depression, which involving numerous systems, the development of anti-depression drugs is extremely slow. Recently, the lower energy metabolism level and impaired synaptic plasticity caused by mitochondrial dysfunction in the pathogenesis of depression is increasingly concerned, and is expected to become a new research target. In our previous study, we have observed that baicalin has a good anti-depression effect, but its mechanism is still not clear. According to the related reports that baicalin can up-regulate the silent information regulator of transcription (SIRT) 1 expression and thus protect the mitochondrial function, we speculated that the anti-depression mechanism of baicalin may be related to that. The present project is planned to establish the animal model of depression using chronic unpredictable mild stress (CUMS). We investigate the anti-depression mechanism of baicalin through the regulation of neuronal function and mitochondrial energy metabolism mediated by AMP-activated protein kinase (AMPK)/SIRT1. The present work will provide a new direction and basis for the development of antidepressants.