Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Department of Anesthesiology, The Yongjia Hospital of TCM, Wenzhou, Zhejiang, China.
Biomed Res Int. 2020 Feb 20;2020:6848450. doi: 10.1155/2020/6848450. eCollection 2020.
To observe the effect of adenosine A1 receptor in the hippocampus of mice on GSK-3 phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.
The model of middle cerebral artery occlusion (MCAO) was established and grouped into electroacupuncture pretreatment group (EA group), MCAO group, and sham-operated group (Sham group). The neurobehavioral manifestation, the volume of cerebral infarction, and its related protein changes in mice in each group were observed. Then, adenosine Α1 receptor antagonist and agonist were injected intraperitoneally to observe the effects of A1 receptor on the phosphorylation level of GSK-3 phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.
(1) Compared with the MCAO group (24 hours after reperfusion), the infarct size in the EA group decreased significantly, and the Garcia neurological score and phosphorylation level of GSK-3 phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury. phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury. phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.
Electroacupuncture pretreatment can increase GSK-3 phosphorylation level via activating A1 receptor, to protect neurons in ischemia-reperfusion injury. phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.
观察小鼠海马腺苷 A1 受体对 GSK-3 磷酸化水平的影响，阐明通过激活 Α1 受体介导脑缺血再灌注损伤的电针预处理的潜在机制。
建立大脑中动脉闭塞（MCAO）模型并分为电针预处理组（EA 组）、MCAO 组和假手术组（Sham 组）。观察各组小鼠的神经行为表现、脑梗死体积及其相关蛋白变化。然后，腹腔内注射腺苷 Α1 受体拮抗剂和激动剂，观察 A1 受体对 GSK-3 磷酸化水平的影响，阐明通过激活 Α1 受体介导脑缺血再灌注损伤的电针预处理的潜在机制。
（1）与 MCAO 组（再灌注 24 小时后）相比，EA 组的梗死体积明显减小，Garcia 神经评分和 GSK-3 磷酸化水平升高。
电针预处理通过激活 A1 受体增加 GSK-3 磷酸化水平，从而保护缺血再灌注损伤中的神经元。
