Wu Zhouquan, Zou Zhiqing, Zou Rong, Zhou Xianju, Cui Suyang
The First Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.
Laboratory of Neurological Diseases, Department of Anesthesiology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
Mol Med Rep. 2015 Jun;11(6):4438-46. doi: 10.3892/mmr.2015.3253. Epub 2015 Jan 26.
Electroacupuncture (EA) pretreatment has been reported to induce tolerance against cerebral ischemia/reperfusion (I/R) injury; however, the mechanisms underlying the beneficial effects of EA remain to be elucidated. Increasing evidence has suggested that excess activation of autophagy is important in I/R injury. The present study aimed to investigate the hypothesis that EA pretreatment‑induced tolerance to cerebral I/R injury was mediated by inhibition of the autophagy pathway. Rats were treated with EA at the acupoint 'Baihui (GV20)' 30 min/day, for five consecutive days prior to the induction of focal cerebral ischemia for 120 min by middle cerebral artery occlusion. Levels of autophagy, cerebral apoptosis, infarct volumes, brain water content and motor deficit were evaluated 12 h following I/R. The autophagy inducer rapamycin was used to investigate the role of autophagy in mediating neuroprotective effects. The results showed that the number of autophagosomes and the expression of the marker proteins of autophagy, including microtubule‑associated protein 1A light chain 3 (LC3)‑II and Beclin 1 were significantly increased 12 h post‑I/R. EA pretreatment decreased the expression of autophagy markers and the number of autophagosomes in the ischemic cortex. In addition, EA pretreatment inhibited neuronal apoptosis, reduced infarct volume and water content, as well as improved neurological outcome of rats following I/R. Furthermore, the reduced expression of LC3‑II and Beclin 1 and the neuroprotective effects were reversed by the autophagy inducer rapamycin. In conclusion, the results of the present study demonstrated that EA pretreatment protected the brain against I/R injury via inhibition of the autophagy process.
据报道，电针预处理可诱导对脑缺血/再灌注（I/R）损伤的耐受性；然而，电针有益作用的潜在机制仍有待阐明。越来越多的证据表明，自噬的过度激活在I/R损伤中起重要作用。本研究旨在探讨电针预处理诱导的脑I/R损伤耐受性是通过抑制自噬途径介导的这一假说。大鼠在“百会（GV20）”穴位接受电针治疗，每天30分钟，连续五天，然后通过大脑中动脉闭塞诱导局灶性脑缺血120分钟。在I/R后12小时评估自噬水平、脑凋亡、梗死体积、脑含水量和运动功能缺损。使用自噬诱导剂雷帕霉素来研究自噬在介导神经保护作用中的作用。结果显示，I/R后12小时，自噬体数量以及自噬标记蛋白的表达，包括微管相关蛋白1A轻链3（LC3）-II和Beclin 1显著增加。电针预处理降低了缺血皮层中自噬标记物的表达和自噬体数量。此外，电针预处理抑制了神经元凋亡，减少了梗死体积和含水量，并改善了I/R后大鼠的神经功能结局。此外，自噬诱导剂雷帕霉素逆转了LC3-II和Beclin 1表达的降低以及神经保护作用。总之，本研究结果表明，电针预处理通过抑制自噬过程保护大脑免受I/R损伤。
