Yang Hui-Jun, Gao Yu, Yun Ji Young, Kim Young Eun, Ehm Gwanhee, Lee Ji Yeon, Yoon Min-Yung, Lee Young-Shin, Kim Han-Joon, Jeon Beomseok
aDepartment of Neurology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan bDepartment of Neurology, Ewha Womans University Mokdong Hospital, Ewha Womans University College of Medicine cDepartment of Neurology and Neuroscience Research Institute, Seoul National University Hospital, Seoul National University College of Medicine dCancer Research Institute, Seoul National University Hospital, Seoul eDepartment of Neurology, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang fDepartment of Neurology, Myongji Hospital, Seonam University College of Medicine, Goyang, Korea gSecond Department of Neurology, The China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, PR China.
Neuroreport. 2017 Jan 1;28(1):50-55. doi: 10.1097/WNR.0000000000000709.
Acupuncture treatment, a complementary and alternative medicine, is associated with a suggested neuroprotective effect in previous preclinical studies of Parkinson's disease (PD); however, results from human clinical trials have been mixed or unsuccessful. Recent systematic reviews of translational neuroprotective studies showed that the supposed efficacy is confounded by low methodological quality, particularly by a lack of randomization and concealed allocation. We sought to replicate previous experimental findings with a study design that mitigates the introduction of bias, including randomization, blinded outcome measures, sham acupuncture application, and allocation concealment by blinded neurotoxin administration. We performed 12 sessions of manual acupuncture at acupoint GB34 (yanglingquan) in mice that were administered the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxin for five consecutive days. In this animal model of PD, acupuncture treatment did not attenuate tyrosine hydroxylase-immunoreactive neuronal death, depletion of striatal dopamine levels, or reduced striatal tyrosine hydroxylase expression. Our results indicate that acupuncture is not neuroprotective against nigrostriatal loss in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of PD.
针灸治疗作为一种补充替代医学，在先前帕金森病（PD）的临床前研究中显示出一定的神经保护作用；然而，人体临床试验的结果却参差不齐或未取得成功。最近对转化神经保护研究的系统评价表明，所谓的疗效受到方法学质量低下的影响，特别是缺乏随机化和分配隐藏。我们试图通过一种减轻偏倚引入的研究设计来复制先前的实验结果，包括随机化、盲法结局测量、假针灸应用以及通过盲法给予神经毒素实现分配隐藏。我们对连续五天给予1-甲基-4-苯基-1,2,3,6-四氢吡啶神经毒素的小鼠，在穴位GB34（阳陵泉）进行了12次手动针灸。在这个PD动物模型中，针灸治疗并未减轻酪氨酸羟化酶免疫反应性神经元死亡、纹状体多巴胺水平的耗竭或纹状体酪氨酸羟化酶表达的降低。我们的结果表明，在亚急性1-甲基-4-苯基-1,2,3,6-四氢吡啶小鼠PD模型中，针灸对黑质纹状体损伤没有神经保护作用。
