Electroacupuncture Produces the Sustained Motor Improvement in 6-Hydroxydopamine-Lesioned Mice.
Electroacupuncture Produces the Sustained Motor Improvement in 6-Hydroxydopamine-Lesioned Mice.
复制标题
电针对 6-羟基多巴胺损伤的小鼠产生持续的运动改善
DOI：
10.1371/journal.pone.0149111
复制
发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Wang X
中科院分区：
文献类型：
--
作者：
Yu Y;Wang K;Deng J;Sun M;Jia J;Wang X
临床和研究证据表明，电针（EA）可促进帕金森病（PD）患者运动功能的恢复。然而，电针治疗的“疗效跨度”，尤其是被认为在停止电针治疗后仍能持续的电针长期效果，尚未得到研究。因此，本研究调查并比较了长期电针应用期间和之后电针对 6-羟基多巴胺 (6-OHDA) 损伤的 PD 小鼠模型运动活动和多巴胺损伤的影响。长期 EA 治疗（每天 30 分钟，每周 6 天，持续 2 或 4 周）可显着减轻运动缺陷并减少多巴胺神经元变性。值得注意的是，电针刺激停止后显示出持久的效果。在 EA 终止后 2 周和 4 周，EA 继续改善 6-OHDA 损伤小鼠的运动功能。与持续的行为效应一致，电针治疗停止后两周，纹状体中的多巴胺周转率持续增加。在这里，我们证明了 EA 的治疗效果超过了 EA 应用的持续时间。在 EA 治疗完成后的较长时间内，EA 能够持续改善 6-OHDA 损伤的 PD 小鼠的运动功能并增强多巴胺的可用性。
Clinical and research evidence has shown that electroacupuncture (EA) promotes recovery of motor function in patients with Parkinson’s disease (PD). However, the “efficacy span” of EA treatment, especially the long-term effect of EA that is thought to last after the cessation of EA treatment, has not been investigated. The present study thus investigated and compared the effect of EA during and after chronic EA application on motor activity and dopamine lesions in a 6-hydroxydopamine (6-OHDA)-lesioned mouse model of PD. Chronic EA treatment (30 min a day, 6 days a week for 2 or 4 weeks) significantly attenuated motor deficiency and reduced dopamine neuron degeneration. Remarkably, EA showed a long-lasting effect after the cessation of EA stimulation. At 2 and 4 weeks after the termination of EA, EA continued to improve motor function in 6-OHDA-lesioned mice. Consistent with sustained behavioral effects, EA induced an enduring increase in the dopamine turnover ratio in the striatum 2 weeks after the cessation of EA treatment. Here we demonstrated that the therapeutic effect of EA outlasted the duration of EA application. During a relatively long period of time after the completion of EA treatment, EA is able to continue to improve motor function and enhance dopamine availability in 6-OHDA-lesioned PD mice.