Neurology Department, (, The Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou 350004, China). 13705042527@126. com.
Neurology Department, (, The Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou 350004, China).
Zhen Ci Yan Jiu. 2023 Nov 25;48(11):1088-1094. doi: 10.13702/j.1000-0607.20230345.
To investigate the mechanism of electroacupuncture (EA) in alleviating cerebral ische-mia injury by activating the Yap-OPA1 signaling axis.
A total of 48 male SD rats were used in the present study. The focal CIRI model was established by occlusion of the middle cerebral artery and reperfusion (MCAO/R), followed by dividing the CIRI rats into model group, EA group and EA+Ver (Verteporfin, Yap antagonist) group (=12 in each group). And another 12 normal rats were used as the sham operation group. For rats of the EA group, EA (4 Hz/20 Hz, 0.5 mA) was applied to "Baihui"(GV20) and "Shenting"(GV24) for 20 min, once daily for 7 days. The neurological deficit score (0 to 4 points) was given according to Longa's method. The infarct volume of rats in each group was assessed by TTC method, and the expression levels of Yes associated protein (Yap), Optic atrophy protein 1 (OPA1), mitofusin 1 (Mfn1), mitofusin 2 (Mfn2) proteins and mRNAs in cerebral cortex of infarcted side, as well as Bax (proapoptotic factor) and Bcl-1 (anti-apoptotic protein) proteins were detected by Westernblot, and real-time PCR, and the immunoactivity of Yap and OPA1 was detected by immunofluorescent staining.
After modeling, the infarct volume, neurological deficit score and the expression of Bax were significantly increased (<0.01), while the mRNA and protein expressions of Yap, OPA1, Mfn2, Mfn1, and Bcl-2 were significantly down-regulated in the model group relevant to the sham operation group (<0.01, <0.05). Compared with the model group, the neurological deficit score, infarct volume and the expression of Bax were significantly decreased (<0.01), while the expression levels of Yap, OPA1, Mfn2, Mfn1 proteins and mRNAs and Bcl-2 protein, Yap and OPA1 immunofluorescence intensify were considerably up-regulated in the EA group (<0.01, <0.05). Following administration of Ver, the effects of EA in down-regulating the neurological score, infarct volume, and Bax expression and up-regulating the expressions of Yap, OPA1, Mfn1, Mfn2 proteins and mRNAs and Yap and OPA1 immunofluorescence intensify were eliminated.
EA of GV20 and GV24 can improve the neurological function in rats with CIRI, which may be associated with its functions in activating mitochondrial fusion function and up-regulating Yap-OPA1 signaling axis.
通过激活 Yap-OPA1 信号轴研究电针对减轻脑缺血损伤的机制。
本研究共使用 48 只雄性 SD 大鼠。通过大脑中动脉闭塞和再灌注（MCAO/R）建立局灶性脑缺血再灌注损伤（CIRI）模型，随后将 CIRI 大鼠分为模型组、电针组和电针+Ver（Verteporfin，Yap 拮抗剂）组（每组 12 只）。另取 12 只正常大鼠作为假手术组。电针组大鼠给予电针（4 Hz/20 Hz，0.5 mA）治疗，取“百会”（GV20）和“神庭”（GV24），每日 1 次，共 7 天。根据 Longa 方法给予神经功能缺损评分（0-4 分）。采用 TTC 法评估各组大鼠的梗死体积，采用 Western blot、实时 PCR 检测梗死侧皮质中 Yes 相关蛋白（Yap）、视神经萎缩蛋白 1（OPA1）、线粒体融合蛋白 1（Mfn1）、线粒体融合蛋白 2（Mfn2）蛋白及其 mRNA 的表达，采用免疫荧光染色检测 Yap 和 OPA1 的免疫活性。
造模后，模型组大鼠的梗死体积、神经功能缺损评分和 Bax 表达显著增加（<0.01），而与假手术组相比，模型组大鼠的 Yap、OPA1、Mfn2、Mfn1 和 Bcl-2 mRNA 和蛋白表达显著下调（<0.01，<0.05）。与模型组相比，电针组大鼠的神经功能缺损评分、梗死体积和 Bax 表达显著降低（<0.01），而电针组大鼠的 Yap、OPA1、Mfn2、Mfn1 蛋白及其 mRNA 和 Bcl-2 蛋白表达以及 Yap 和 OPA1 免疫荧光强度显著升高（<0.01，<0.05）。给予 Ver 后，电针下调神经评分、梗死体积和 Bax 表达，上调 Yap、OPA1、Mfn1、Mfn2 蛋白及其 mRNA 和 yap 和 OPA1 免疫荧光强度的作用被消除。
电针 GV20 和 GV24 可改善 CIRI 大鼠的神经功能，其作用可能与其激活线粒体融合功能和上调 yap-OPA1 信号轴有关。
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