Wang Jinjin, Ma Qinqin, Li Fang, Yuan Zhengzhong, Li Haiyan, Fu Wenbin
Department of Rehabilitation Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
The Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Curr Neurovasc Res. 2025 Aug 11. doi: 10.2174/0115672026381025250803030921.
Post-stroke dysphagia (PSD) is a common complication after acute stroke. It can be effectively alleviated by electroacupuncture (EA) stimulation at the Baihui acupoint; however, the underlying mechanism remains unclear.
Male ICR mice were used, and the suture occlusion method was employed to establish the middle cerebral artery occlusion (MCAO) mouse model. EA stimulation was applied to the Baihui acupoint for intervention. After treatment, the survival rate of the mice was assessed. Subsequently, a water swallow test was conducted to evaluate the degree of dysphagia in the mice. Additionally, neurological function was assessed through Garcia scoring and measurement of serum Ca2+-Mg2+-ATPase activity. Fur-thermore, MRI was utilized to evaluate the therapeutic effects of EA on cerebral infarction and edema rates. Then, the antioxidant activity of the EA intervention was assessed by measuring indicators of oxida-tive damage. Finally, the expressions of gamma- aminobutyric acid type B receptor subunit 1 (GAB-ABR1), N-methyl-D-aspartate receptor 1 (NMDAR1) were detected through WB, RT-qPCR, and immu-nofluorescence.
EA intervention effectively increased the survival rate of MCAO mice and alleviated their dysphagia. Additionally, the impaired neurological function of the mice was improved, and cerebral infarction and edema rates were reduced. Furthermore, EA alleviated oxidative stress in mice, reduced damage to neurons in the nucleus ambiguus, and upregulated GABABR1 while downregulating NMDAR1.
Although we suggested that EA may exert therapeutic activity for PSD by maintaining the balance of NMDAR1 and GABABR1, this conclusion still requires further experimental validation.
EA stimulation of the Baihui acupoint was effective in treating PSD, which was related to its ability to improve damaged neurons, upregulate GABABR1, and downregulate NMDAR1. These findings provided a new insight into the mechanisms of EA treatment for PSD and serve as a theoretical basis for future clinical research.
中风后吞咽困难（PSD）是急性中风后的常见并发症。电针（EA）刺激百会穴可有效缓解该症状，但其潜在机制尚不清楚。
选用雄性ICR小鼠，采用线栓法建立大脑中动脉闭塞（MCAO）小鼠模型。应用EA刺激百会穴进行干预。治疗后，评估小鼠的存活率。随后，进行水吞咽试验以评估小鼠的吞咽困难程度。此外，通过Garcia评分和血清Ca2+-Mg2+-ATPase活性测定评估神经功能。此外，利用MRI评估EA对脑梗死和水肿率的治疗效果。然后，通过测量氧化损伤指标评估EA干预的抗氧化活性。最后，通过蛋白质免疫印迹法（WB）、逆转录-定量聚合酶链反应（RT-qPCR）和免疫荧光检测γ-氨基丁酸B型受体亚基1（GAB-ABR1）、N-甲基-D-天冬氨酸受体1（NMDAR1）的表达。
EA干预有效提高了MCAO小鼠的存活率，缓解了其吞咽困难。此外，改善了小鼠受损的神经功能，降低了脑梗死和水肿率。此外，EA减轻了小鼠的氧化应激，减少了疑核神经元的损伤，上调了GABABR1，同时下调了NMDAR1。
尽管我们认为EA可能通过维持NMDAR1和GABABR1的平衡对PSD发挥治疗作用，但这一结论仍需进一步的实验验证。
电针刺激百会穴治疗PSD有效，这与其改善受损神经元、上调GABABR1和下调NMDAR1的能力有关。这些发现为EA治疗PSD的机制提供了新的见解，并为未来的临床研究提供了理论依据。
