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Electroacupuncture Intervention Improves Post-Stroke Dysphagia by Modulating NMDAR1 and GABABR1
Jinjin Wang1,2, Qinqin Ma1, Fang Li1
1Department of Rehabilitation Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Electroacupuncture (EA) stimulation effectively treats post-stroke dysphagia (PSD) by improving neuronal damage and balancing specific receptors. This study elucidates the mechanism behind EA
Area of Science:
- Neuroscience
- Acupuncture Research
- Stroke Rehabilitation
Background:
- Post-stroke dysphagia (PSD) is a frequent complication following acute stroke.
- Electroacupuncture (EA) stimulation at the Baihui acupoint shows promise for alleviating PSD, but its mechanism is not fully understood.
Purpose of the Study:
- To investigate the therapeutic mechanisms of EA stimulation at the Baihui acupoint for treating post-stroke dysphagia (PSD).
- To evaluate the effects of EA on neurological function, cerebral infarction, edema, and oxidative stress in a mouse model of stroke.
Main Methods:
- A middle cerebral artery occlusion (MCAO) mouse model was established to induce stroke.
- EA stimulation was applied to the Baihui acupoint, followed by assessments of survival rate, swallowing function, neurological scores, and serum Ca2+-Mg2+-ATPase activity.
- Magnetic resonance imaging (MRI) evaluated cerebral infarction and edema, while oxidative stress markers were measured.
- Western blot, RT-qPCR, and immunofluorescence detected the expression of gamma-aminobutyric acid type B receptor subunit 1 (GABABR1) and N-methyl-D-aspartate receptor 1 (NMDAR1).
Main Results:
- EA intervention significantly increased survival rates and alleviated dysphagia in MCAO mice.
- Neurological function improved, and rates of cerebral infarction and edema decreased following EA treatment.
- EA reduced oxidative stress, protected neurons in the nucleus ambiguus, upregulated GABABR1, and downregulated NMDAR1.
Conclusions:
- EA stimulation of the Baihui acupoint is effective in treating PSD.
- The therapeutic effects are linked to improved neuronal integrity and a balanced expression of GABABR1 and NMDAR1.
- These findings offer new insights into EA's mechanism for PSD and provide a basis for future clinical research.
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