Deng Jiahui, Lv E, Yang Jian, Gong Xiaoli, Zhang Wenzhong, Liang Xibin, Wang Jiazeng, Jia Jun, Wang Xiaomin
Departments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China.
Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, 94305, USA.
J Neuroinflammation. 2015 May 28;12:103. doi: 10.1186/s12974-015-0302-z.
The acupuncture or electroacupuncture (EA) shows the therapeutic effect on various neurodegenerative diseases. This effect was thought to be partially achieved by its ability to alleviate existing neuroinflammation and glial dysfunction. In this study, we systematically investigated the effect of EA on abnormal neurochemical changes and motor symptoms in a mouse neurodegenerative disease model.
The transgenic mouse which expresses a mutant α-synuclein (α-syn) protein, A53T α-syn, in brain astrocytic cells was used. These mice exhibit extensive neuroinflammatory and motor phenotypes of neurodegenerative disorders. In this study, the effects of EA on these phenotypic changes were examined in these mice.
EA improved the movement detected in multiple motor tests in A53T mutant mice. At the cellular level, EA significantly reduced the activation of microglia and prevented the loss of dopaminergic neurons in the midbrain and motor neurons in the spinal cord. At the molecular level, EA suppressed the abnormal elevation of proinflammatory factors (tumor necrosis factor-α and interleukin-1β) in the striatum and midbrain of A53T mice. In contrast, EA increased striatal and midbrain expression of a transcription factor, nuclear factor E2-related factor 2, and its downstream antioxidants (heme oxygenase-1 and glutamate-cysteine ligase modifier subunits).
These results suggest that EA possesses the ability to ameliorate mutant α-syn-induced motor abnormalities. This ability may be due to that EA enhances both anti-inflammatory and antioxidant activities and suppresses aberrant glial activation in the diseased sites of brains.
针刺或电针(EA)对多种神经退行性疾病具有治疗作用。这种作用被认为部分是通过其减轻现有神经炎症和神经胶质细胞功能障碍的能力来实现的。在本研究中,我们系统地研究了电针对小鼠神经退行性疾病模型中异常神经化学变化和运动症状的影响。
使用在脑星形胶质细胞中表达突变α-突触核蛋白(α-syn)A53T α-syn的转基因小鼠。这些小鼠表现出神经退行性疾病广泛的神经炎症和运动表型。在本研究中,检测了电针对这些小鼠这些表型变化的影响。
电针改善了A53T突变小鼠在多项运动测试中检测到的运动能力。在细胞水平上,电针显著降低了小胶质细胞的激活,并防止了中脑多巴胺能神经元和脊髓运动神经元的丢失。在分子水平上,电针抑制了A53T小鼠纹状体和中脑促炎因子(肿瘤坏死因子-α和白细胞介素-1β)的异常升高。相反,电针增加了转录因子核因子E2相关因子2及其下游抗氧化剂(血红素加氧酶-1和谷氨酸-半胱氨酸连接酶修饰亚基)在纹状体和中脑的表达。
这些结果表明,电针具有改善突变α-syn诱导的运动异常的能力。这种能力可能是由于电针增强了抗炎和抗氧化活性,并抑制了脑病变部位异常的神经胶质细胞激活。