电针广泛用于治疗脑梗塞，但机制仍不明确。自噬在电针脑缺血耐受的作用是目前研究的热点。Inoki研究表明阻断Wnt信号可促进自噬调控蛋白mTOR水解，增加自噬发生。课题组发现Wnt信号参与了电针脑缺血耐受，而阻断Wnt通路第二信使β-catenin可逆转电针效应。但电针、Wnt/β-catenin通路、自噬三者如何相互作用介导脑缺血耐受，尚无类似研究。因此，课题组提出科学假说：电针通过激活Wnt信号，抑制β-catenin降解，增加mTOR含量，从而减少自噬发生，达到脑缺血耐受。本研究拟建立LPR6KO与WT MCAO小鼠以及神经元OGD/Rep模型，分别运用TUNEL、WB、细胞培养和病毒转染等技术，观察行为学、自噬标记蛋白、凋亡与自噬体等指标变化，分别从整体、细胞、分子等不同层面，论证Wnt/β-catenin通路调控自噬介导电针脑缺血耐受。本研究将为电针治疗脑梗塞提供科学依据。

Electroacupuncture(EA) is widely used in the treatment of cerebral infarction, but the mechanism remains unclear. The function of autophagy in cerebral ischemic tolerance of EA is the central issue of current research. Inoki’ s study suggested that blocking Wnt signaling could prohydrolyze mTOR which can regulate the autophagy, and increased autophagy. We found that Wnt signaling involved in the cerebral ischemic tolerance of EA, while blocking beta-catenin in Wnt signaling could reverse the function of EA. Whether the effect of cerebral ischemic tolerance could be mediated by EA，Wnt/ beta-catenin and autophagy, there was no interrelate research. So we propose scientific hypothesis: EA can activate Wnt signaling, which can inhibit the degradation of beta-catenin and increase mTOR content, thereby the autophagy of neuron can be reduced, then EA can achieve cerebral ischemic tolerance. We will establish LPR6 konckout and wild type (WT) middle cerebral artery occlusion (MCAO) mice and Neuron Oxygen and glucose deprivation (OGD) / reperfusion model. We will respectively use TUNEL, Western blot, cell culture and viral transfection technology and observe the changes of behavioristics, apoptosis , autophagy, autophagy protein and other indicators. We will demonstrate that the Wnt / beta-catenin signaling can regulate autophagy in mediating cerebral ischemia tolerance of EA by the changes of Wnt signaling proteins, apoptosis , autophagy, autophagy protein and other indicators. This research will provide scientific basis for EA treatment of cerebral infraction.