Neferine is the major alkaloid compound isolated from the seed embryos of lotus. Neferine has many pharmacological effects, such as anti-inflammatory, antioxidative stress, and antiapoptotic effects, and it maintains autophagic balance. The purpose of this study was to explore the mechanism by which neferine attenuates autophagy after permanent cerebral ischemia in rats. We performed permanent cerebral ischemia in rats by middle cerebral artery occlusion (pMCAO) for 12 h with or without administration of neferine or nimodipine, a calcium (Ca²⁺) channel blocker. Neuroprotective effects were determined by evaluating the infarct volume and neurological deficits. Autophagy and its signaling pathway were determined by evaluating the expression of phosphorylated AMP-activated protein kinase alpha (AMPKα), phosphorylated mammalian target of rapamycin (mTOR), beclin-1, microtubule-associated protein 1A/1B-light chain 3 class II (LC3-II), and p62 by western blotting. Autophagosomes were evaluated by transmission electron microscopy. Neferine treatment significantly reduced infarct volumes and improved neurological deficits. Neferine significantly attenuated the upregulation of autophagy-associated proteins such as LC3-II, beclin-1, and p62 as well as autophagosome formation, all of which were induced by pMCAO. Neferine exerted remarkable protection against cerebral ischemia, possibly via the regulation of autophagy mediated by the Ca²⁺-dependent AMPK/mTOR pathway.

Neferine 是从莲花种子胚中分离出来的主要生物碱化合物。Neferine具有许多药理作用，如抗炎、抗氧化应激和抗凋亡作用，并维持自噬平衡。本研究的目的是探讨脑啡肽减轻大鼠永久性脑缺血后自噬的机制。我们通过大脑中动脉闭塞 (pMCAO) 对大鼠进行永久性脑缺血 12 小时，同时给予或不给予奈菲林或尼莫地平，一种钙 (Ca ²⁺) 频道拦截器。通过评估梗塞体积和神经功能缺损来确定神经保护作用。通过评估磷酸化 AMP 活化蛋白激酶 α (AMPKα)、磷酸化哺乳动物雷帕霉素靶蛋白 (mTOR)、beclin-1、微管相关蛋白 1A/1B-轻链 3 类 II 的表达来确定自噬及其信号通路。 LC3-II) 和 p62 通过蛋白质印迹。通过透射电子显微镜评估自噬体。Neferine 治疗显着减少了梗死体积并改善了神经功能缺损。Neferine 显着减弱了自噬相关蛋白（如 LC3-II、beclin-1 和 p62）的上调以及自噬体的形成，所有这些都是由 pMCAO 诱导的。Neferine 对脑缺血有显着的保护作用，²⁺依赖性 AMPK/mTOR 通路。