首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Electroacupuncture Promotes Recovery of Motor Function and Reduces Dopaminergic Neuron Degeneration in Rodent Models of Parkinson’s Disease
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Electroacupuncture Promotes Recovery of Motor Function and Reduces Dopaminergic Neuron Degeneration in Rodent Models of Parkinson’s Disease

机译:电针可促进帕金森氏病啮齿动物模型的运动功能恢复并减少多巴胺能神经元变性

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摘要

Parkinson’s disease (PD) is a common neurodegenerative disease. The pathological hallmark of PD is a progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta in the brain, ultimately resulting in severe striatal dopamine deficiency and the development of primary motor symptoms (e.g., resting tremor, bradykinesia) in PD. Acupuncture has long been used in traditional Chinese medicine to treat PD for the control of tremor and pain. Accumulating evidence has shown that using electroacupuncture (EA) as a complementary therapy ameliorates motor symptoms of PD. However, the most appropriate timing for EA intervention and its effect on dopamine neuronal protection remain unclear. Thus, this study used the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model (systemic-lesioned by intraperitoneal injection) and the 1-methyl-4-phenylpyridinium (MPP+)-lesioned rat model (unilateral-lesioned by intra-SN infusion) of PD, to explore the therapeutic effects and mechanisms of EA at the GB34 (Yanglingquan) and LR3 (Taichong) acupoints. We found that EA increased the latency to fall from the accelerating rotarod and improved striatal dopamine levels in the MPTP studies. In the MPP+ studies, EA inhibited apomorphine induced rotational behavior and locomotor activity, and demonstrated neuroprotective effects via the activation of survival pathways of Akt and brain-derived neurotrophic factor (BDNF) in the SN region. In conclusion, we observed that EA treatment reduces motor symptoms of PD and dopaminergic neurodegeneration in rodent models, whether EA is given as a pretreatment or after the initiation of disease symptoms. The results indicate that EA treatment may be an effective therapy for patients with PD.
机译:帕金森氏病(PD)是一种常见的神经退行性疾病。 PD的病理特征是大脑黑质(SN)致密性黑质中多巴胺能神经元的逐渐丧失,最终导致PD中严重的纹状体多巴胺缺乏和原发性运动症状(例如静息性震颤,运动迟缓)的发展。针灸长期以来一直用于中药治疗PD,以控制震颤和疼痛。越来越多的证据表明,使用电针(EA)作为补充疗法可改善PD的运动症状。但是,EA干预的最合适时机及其对多巴胺神经元保护的作用仍不清楚。因此,本研究使用了1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)损伤的小鼠模型(通过腹膜内注射全身性损伤)和1-甲基-4-苯基吡啶鎓(MPP < sup> + )损伤的PD大鼠模型(单侧SN内损伤),以探讨EA对GB34(阳陵泉)和LR3(太冲)穴的治疗作用和机制。我们发现,在MPTP研究中,EA增加了从加速的旋转脚架跌落的潜伏期,并改善了纹状体多巴胺水平。在MPP + 研究中,EA抑制了阿扑吗啡诱导的旋转行为和自发活动,并通过激活SN区Akt和脑源性神经营养因子(BDNF)的生存途径证明了神经保护作用。总之,我们观察到,EA可以减轻啮齿动物模型中PD的运动症状和多巴胺能神经退行性变,无论EA是作为预处理剂还是在疾病症状发作后使用。结果表明,EA治疗可能是PD患者的有效疗法。

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