Parkinson’s disease (PD) is characterized by dopaminergic neuron loss in the substantia nigra. However, specific sensory stimulation via electroacupuncture (EA) therapy may attenuate this loss by promoting the expression of endogenous neurotrophic factors in a manner similar to physical therapy. We investigated the potential protective effects of EA on dopaminergic neurons in a mouse model of PD and whether these effects are associated with the promotion of endogenous brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Mouse models of PD were generated using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine. Motor performance was assessed using behavioral tests, and Western blot experiments, enzyme-linked immunosorbent assays (ELISAs), and immunohistochemical assays were performed. In both mouse models, EA treatment ameliorated motor impairments and dopaminergic neuron loss; these changes were accompanied by increases in BDNF and GDNF. In the MPTP group, EA treatment improved motor dysfunction by attenuating dopaminergic neuron loss in the substantia nigra, similar to the effects of levodopa. EA treatment significantly upregulated BDNF and GDNF expression in both the substantia nigra and striatum. Moreover, EA treatment induced the expression of cAMP response element binding protein (CREB) as well as Akt and Pitx3 in dopaminergic neurons in the substantia nigra. However, levodopa treatment did not induce BDNF/GDNF activation or related signaling factors. Thus, EA therapy may exert protective effects on dopaminergic neurons by upregulating the expression of BDNF, GDNF, and related signaling factors, thereby improving motor function. Hence, EA may represent an effective adjuvant therapy for motor deficits in patients with PD.

中文翻译：

---

电针疗法通过帕金森氏病小鼠模型通过脑源性神经营养因子和胶质细胞系源性神经营养因子改善运动功能障碍

帕金森氏病（PD）的特征是黑质中的多巴胺能神经元丢失。但是，通过类似于物理疗法的方式，通过电针（EA）治疗的特定感觉刺激可以通过促进内源性神经营养因子的表达来减轻这种损失。我们调查了EA对PD小鼠模型中多巴胺能神经元的潜在保护作用，以及这些作用是否与促进内源性脑源性神经营养因子（BDNF）和神经胶质细胞系源性神经营养因子（GDNF）相关。PD的小鼠模型是使用1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）和6-羟基多巴胺生成的。使用行为测试，蛋白质印迹实验，酶联免疫吸附测定（ELISA）评估运动能力，并进行免疫组织化学分析。在这两种小鼠模型中，电针治疗均能改善运动障碍和多巴胺能神经元丢失。这些变化伴随着BDNF和GDNF的增加。在MPTP组中，EA治疗通过减轻黑质中的多巴胺能神经元损失来改善运动功能障碍，类似于左旋多巴的作用。EA处理显着上调了黑质和纹状体中BDNF和GDNF的表达。此外，EA处理诱导了黑质中多巴胺能神经元中cAMP反应元件结合蛋白（CREB）以及Akt和Pitx3的表达。但是，左旋多巴治疗并未诱导BDNF / GDNF激活或相关信号转导因子。因此，电针疗法可能通过上调BDNF，GDNF的表达而对多巴胺能神经元产生保护作用，和相关的信号传导因子，从而改善运动功能。因此，EA可能代表PD患者运动缺陷的有效辅助治疗。