Dai Qin-Xue, Geng Wu-Jun, Zhuang Xiu-Xiu, Wang Hong-Fa, Mo Yun-Chang, Xin He, Chen Jiang-Fan, Wang Jun-Lu
Department of Anesthesiology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Department of Neurology, Boston University School of Medicine, Boston, MA, USA.
Neural Regen Res. 2017 Feb;12(2):228-234. doi: 10.4103/1673-5374.200806.
The activation of adenosine A1 receptors is important for protecting against ischemic brain injury and pretreatment with electroacupuncture has been shown to mitigate ischemic brain insult. The aim of this study was to test whether the adenosine A1 receptor mediates electroacupuncture pretreatment-induced neuroprotection against ischemic brain injury. We first performed 30 minutes of electroacupuncture pretreatment at the acupoint (GV20), delivered with a current of 1 mA, a frequency of 2/15 Hz, and a depth of 1 mm. High-performance liquid chromatography found that adenosine triphosphate and adenosine levels peaked in the cerebral cortex at 15 minutes and 120 minutes after electroacupuncture pretreatment, respectively. We further examined the effect of 15 or 120 minutes electroacupuncture treatment on ischemic brain injury in a rat middle cerebral artery-occlusion model. We found that at 24 hours reperfusion,120 minutes after electroacupuncture pretreatment, but not for 15 minutes, significantly reduced behavioral deficits and infarct volumes. Last, we demonstrated that the protective effect gained by 120 minutes after electroacupuncture treatment before ischemic injury was abolished by pretreatment with the A1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (1 mg/kg, intraperitoneally). Our results suggest that pretreatment with electroacupuncture at the acupoint elicits protection against transient cerebral ischemia action at adenosine A1 receptors.
腺苷A1受体的激活对于预防缺血性脑损伤很重要,并且已证明电针预处理可减轻缺血性脑损伤。本研究的目的是测试腺苷A1受体是否介导电针预处理诱导的对缺血性脑损伤的神经保护作用。我们首先在穴位(GV20)进行了30分钟的电针预处理,电流为1 mA,频率为2/15 Hz,深度为1 mm。高效液相色谱法发现,电针预处理后15分钟和120分钟时,大脑皮层中的三磷酸腺苷和腺苷水平分别达到峰值。我们进一步研究了15分钟或120分钟电针治疗对大鼠大脑中动脉闭塞模型缺血性脑损伤的影响。我们发现,在再灌注24小时时,电针预处理120分钟后,而非15分钟后,显著减少了行为缺陷和梗死体积。最后,我们证明,在缺血性损伤前120分钟电针治疗所获得的保护作用被A1受体拮抗剂8-环戊基-1,3-二丙基黄嘌呤(1 mg/kg,腹腔注射)预处理所消除。我们的结果表明,在穴位进行电针预处理可通过腺苷A1受体发挥对短暂性脑缺血的保护作用。