Electroacupuncture alleviated post-stroke cognitive impairment via the mTOR/NLRP3-mediated autophagy-inflammatory pathway

被引:3
作者
Lang, Jiawang [1 ]
Luo, Jianchang [1 ]
Lang, Jiachen [2 ]
Wang, Luodan [1 ]
Xu, Wenbin [1 ]
Jia, Jie [3 ]
Zhao, Zhipeng [4 ]
Lang, Boxu [1 ]
机构
[1] Taizhou Municipal Hosp, Dept Rehabil Med, 381-1 Zhongshan East Rd, Taizhou 318000, Zhejiang, Peoples R China
[2] Guizhou Univ Tradit Chinese Med, Acupuncture & Massage Coll, Dept Acupuncture & Massage Dept, Guiyang 550025, Guizhou, Peoples R China
[3] Fudan Univ, Dept Rehabil Med, Jinshan Hosp Affiliated, Shanghai 200000, Peoples R China
[4] Taizhou Univ, Sch Med, Dept Rehabil Med, Taizhou 318000, Zhejiang, Peoples R China
关键词
Post-stroke cognitive impairment; mTOR/NLRP3; pathway; Apoptosis; Inflammation; Autophagy;
D O I
10.1186/s40001-024-02131-9
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
BackgroundPost-stroke cognitive impairment (PSCI) severely reduces quality of life of patients with stroke. This study aimed to assess the effects of electroacupuncture (EA) on PSCI and the role of the mTOR/NLRP3-mediated autophagy-inflammatory pathway in this process.MethodsThe rat focal cerebral ischemia model was established using middle cerebral artery occlusion (MCAO). Following successful induction of the model, EA was applied to the bilateral Fengchi, Fengfu, and Dazhui acupoints, and brain tissue samples were collected on day 15. Cognitive function was assessed using the Morris water maze test. Cerebral infarct volume was quantified by Triphenyltetrazolium chloride (TTC) staining. Hematoxylin-eosin and TUNEL staining were performed to evaluate pathological changes and apoptosis rates. Apoptosis-, inflammation-, and autophagy-related biomarkers were measured, and autophagosomes were visualized using transmission electron microscopy.ResultsMCAO rats exhibited slower weight gain, reduced mobility, increased infarct size, pathological damage, and apoptosis, confirming successful establishment of the MCAO rat model. Following EA treatment, MCAO rats displayed faster weight gain, improved mobility, and shorter escape latency. EA also reduced the area of cerebral infarction and alleviated pathological damage and apoptosis in MCAO rats. Furthermore, EA downregulated IL-1 beta, IL-18, NLRP3, and LC3 II/LC3 I expression and upregulated p62, mTOR, and Beclin-1 expression in MCAO rats. EA treatment also decreased the number of autophagosomes in these rats.ConclusionsEA effectively mitigates post-stroke cognitive impairment by reducing apoptosis, inflammation, and autophagy through the regulation of the mTOR/NLRP3-mediated autophagy-inflammatory pathway, offering valuable therapeutic insights for stroke rehabilitation.
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页数:10
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