基于线粒体自噬途径探索柚皮素对脑缺血再灌注损伤的神经保护作用

缺血性脑血管病是一种严重影响人类健康的疾病，寻找有效的神经保护药物和治疗靶点是当前科技和医务工作者的迫切任务。线粒体自噬途径被认为是脑缺血再灌注病理过程中内源性的保护机制，而PINK1/Parkin通路是目前公认的调控细胞线粒体自噬重的经典信号通路，是缺血性脑血管病防治的潜在靶点。中药枳实和陈皮的有效成分柚皮素已被证实具有显著的抗氧化药理作用，我们的前期研究发现柚皮素对缺血再灌注后神经细胞具有线粒体保护和抗氧化应激作用。然而柚皮素是否通过影响线粒体自噬途径发挥其线粒体保护、抗氧化应激和神经保护作用，国内外均未见文献报道。因此，本项目拟通过体外神经细胞培养和动物模型，从PINK1/Parkin通路介导的线粒体自噬途径探索柚皮素的神经保护作用。

Ischemic cerebrovascular disease is a serious disease affecting human health,finding effective neuroprotective drugs and therapeutic targets is an urgent task for current scientific and medical workers. Mitochondrial autophagy pathway is considered as an endogenous protective mechanism in the pathological process of cerebral ischemia-reperfusion, and PINK1/Parkin pathway is currently recognized as the classic signal pathway regulating mitochondrial autophagy weight is the prevention and treatment of ischemic cerebrovascular disease Potential target.Naringin and dried tangerine peel active ingredient naringenin has been shown to have significant anti-oxidative pharmacological effects, our previous study has found that naringenin on mitochondria after ischemia-reperfusion injury and anti-oxidative stress. However, whether naringenin exerts its mitochondrial protection, anti-oxidative stress and neuroprotective effects by affecting mitochondrial autophagy, is still unclear. Therefore, this project intends to explore the neuroprotective effects of naringenin from the mitochondrial autophagy mediated by the PINK1/Parkin pathway through in vitro and vivo study.