线粒体参与脑缺血损伤的多个环节，是临床中风治疗的新希望。适度的线粒体自噬可防止凋亡触发，减轻细胞损伤。最新研究发现线粒体上存在大麻素受体mtCB1，调节其呼吸和能量代谢、钙稳态及细胞凋亡。而我们发现内源性大麻素系统是电针脑保护作用的关键机制之一；进一步预实验显示：电针可调节线粒体功能，激活mtCB1不仅有脑和线粒体保护作用，还上调线粒体自噬相关蛋白PINK1表达，提示电针可能通过mtCB1作用PINK1/PARKIN通路，促进损伤线粒体自噬，调节线粒体功能，从而减轻脑缺血性损伤。本项目拟以mtCB1为靶点，应用基因敲除小鼠、免疫电镜、RNA干扰等技术，研究电针通过mtCB1调节中风后损伤线粒体自噬的作用，探索电针通过mtCB1作用于 PINK1/ PARKIN通路调控线粒体自噬，发挥脑保护作用的分子机制，从而为中风后线粒体功能调节提供新的治疗靶点，为针刺治疗缺血性脑中风提供新的理论依据。

Involved in cerebral ischemia-reperfusion (I/R) injury, mitochondria is an exciting target of clinically translatable therapeutics. Appropriate regulation of mitochondrial autophagy(mitophagy) would inhibit the onset of apoptosis, attenuate the cellular I/R injury. And the recent published research showed that type-1 cannabinoid receptor (CB1) is present at the membranes of mouse neuronal mitochondria (mtCB1), where it directly controls cellular respiration, energy production, calcium homeostasis and apoptosis. Meanwhile, the upregulation of endocanabinoids system (ECS) is one of the central mechanisms of neuroprotective effect induced by elctroacupuncture(EA). Our preliminary experiments shown that EA could regulate mitochondrial function, merely activation of mtCB1 could significantly increase the activity of neurons with oxygen-glucose deprivation injury, and up-regulate the expression of PINK1 which is a crucial factor associated with selective mitophagy. Therefore, we speculate that mtCB1 is essential for neuroprotective effect induced by EA, activation of mtCB1 will regulate mitophagy through PINK/PARKIN pathway, and finally result in inhibition of mitochondrial dysfunction and neuroprotective effect. Mitochondrial CB1 knockout mice, immunoelectron microscopy, and siRNA techniques will be used in this study to investigate the regulating effect of mitophagy induced by EA through mtCB1, to confirm the molecular mechanisms that mtCB1 regulates mitophagy through PINK1/PARKIN to attenuate ischemia reperfusion injury. The present study is aimed to represent a promising therapeutic target for treatment of stroke, and provide novel evidence and insights on the neuroprotective effect induced by EA.