Kang Mengru, Cai Jianbin, Yi Weimin, Zhang Bin, Ai Liang, Ning Baile, Dong Jiayi, Chen Liudan, Fu Wenbin
The Second Clinical College of Guangzhou University of Chinese Medicine Guangzhou, Guangdong, China.
Department of Traditional Chinese Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sun University Guangzhou, Guangdong, China.
Am J Transl Res. 2025 May 15;17(5):3619-3629. doi: 10.62347/PGKC2376. eCollection 2025.
To explore the therapeutic effects and potential mechanism of electroacupuncture (EA) in a Parkinson's disease (PD) mouse model.
C57BL/6 mice were randomly assigned to control, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), MPTP + sham EA, and MPTP + EA groups. PD was induced by MPTP. EA was applied at Baihui (GV20), Hegu (LI4), and Taichong (LR3). After 20 days of treatment, behavioral tests including the open field test, rotarod test, and Morris water maze were conducted. Dopaminergic neuron survival, apoptosis, and expression of inflammatory markers were assessed.
MPTP-induced mice exhibited impaired motor and cognitive performance, increased brain apoptosis, reduced dopaminergic neurons, and elevated expression of α-synuclein, NLRP3, IL-1β, IL-18, caspase-1, and gasdermin D. These changes were not significantly altered by sham EA. In contrast, EA significantly improved motor and cognitive function, reduced apoptosis, preserved dopaminergic neurons, increased tyrosine hydroxylase expression, and suppressed NLRP3 inflammasome activation.
EA mitigates PD symptoms and exerts neuroprotective effects by inhibiting NLRP3 inflammasome-mediated neuroinflammation.
探讨电针(EA)对帕金森病(PD)小鼠模型的治疗作用及潜在机制。
将C57BL/6小鼠随机分为对照组、1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)组、MPTP + 假电针组和MPTP + 电针组。通过MPTP诱导建立PD模型。电针选取百会(GV20)、合谷(LI4)和太冲(LR3)穴位。治疗20天后,进行旷场试验、转棒试验和莫里斯水迷宫等行为学测试。评估多巴胺能神经元的存活、凋亡以及炎症标志物的表达。
MPTP诱导的小鼠表现出运动和认知功能受损、脑凋亡增加、多巴胺能神经元减少以及α-突触核蛋白、NLRP3、白细胞介素-1β、白细胞介素-18、半胱天冬酶-1和gasdermin D表达升高。假电针未显著改变这些变化与之形成对比的是,电针显著改善了运动和认知功能,减少了凋亡,保护了多巴胺能神经元,增加了酪氨酸羟化酶的表达,并抑制了NLRP3炎性小体的激活。
电针通过抑制NLRP3炎性小体介导的神经炎症减轻PD症状并发挥神经保护作用。