Wu G, Li L, Li H-M, Zeng Y, Wu W-C
Institute of Biomedical Engineering, School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, 610041 Sichuan, P. R. China.
Laboratory of Cardiovascular Diseases, Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, 610041 Sichuan, P. R. China.
Cell Mol Biol (Noisy-le-grand). 2017 Apr 29;63(4):38-45. doi: 10.14715/cmb/2017.63.4.7.
Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by progressive deterioration of cognition and memory, in which oxidative stress has been played a crucial role in the pathology of AD. Electroacupuncture (EA) is a widely used therapy based on traditional acupuncture combined with modern electrotherapy in Asia. The present study aimed to determine the effects of EA treatment on spatial learning and memory impairment, and to elucidate the status of NOX2-related oxidative stress in a rat model of Alzheimer's disease induced by Beta-amyloid1-42 (Aβ1-42). Fifty-six adult female Sprague-Dawley (SD) rats were randomly divided into four groups: sham, sham+EA, AD and AD+EA. The rats in Sham+EA and AD+EA groups were respectively administrated EA treatment at Baihui and yongquan acupoints, once a day for 30 min, lasting for 28 days. The spatial learning and memory functions were assessed by Morris water maze (MWM) test. The activities of total antioxidant capacity (T-AOC), reactive oxygen species (ROS), malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OH-dG) were evaluated. Moreover, the neuronal injury was detected by Nissl staining. Meanwhile, the NeuN expression was examined in the hippocampus, the expression levels of Nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase2(NOX2) was detected by immunofluorescence staining and western blot. The results showed that EA treatment significantly improved spatial learning and memory impairment in rats induced by Aβ1-42. Concomitantly, EA treatment markedly restored T-AOC and attenuated the abnormal increase in levels of ROS, MDA and 8-OH-dG in the hippocampus of the AD rats. More notably, EA treatment also effectively ameliorated neuronal injury and counteracted the aberrant increase of NOX2 levels in the hippocampus of AD rats. Our findings suggested that EA is a potential strategy for the treatment of AD, and the possible mechanism is associated with the alleviation of neuronal injury and inhibition of NOX2-related oxidative stress.
阿尔茨海默病（AD）是一种慢性神经退行性疾病，其特征为认知和记忆功能进行性衰退，其中氧化应激在AD病理学中起关键作用。电针（EA）是一种在亚洲广泛应用的疗法，它基于传统针灸并结合现代电疗法。本研究旨在确定电针治疗对空间学习和记忆障碍的影响，并阐明β-淀粉样蛋白1-42（Aβ1-42）诱导的阿尔茨海默病大鼠模型中与NADPH氧化酶2（NOX2）相关的氧化应激状态。56只成年雌性Sprague-Dawley（SD）大鼠被随机分为四组：假手术组、假手术+电针组、AD组和AD+电针组。假手术+电针组和AD+电针组的大鼠分别在百会穴和涌泉穴进行电针治疗，每天一次，每次30分钟，持续28天。通过莫里斯水迷宫（MWM）试验评估空间学习和记忆功能。评估总抗氧化能力（T-AOC）、活性氧（ROS）、丙二醛（MDA）和8-羟基-2'-脱氧鸟苷（8-OH-dG）的活性。此外，通过尼氏染色检测神经元损伤。同时检测海马区NeuN的表达，通过免疫荧光染色和蛋白质印迹法检测烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶2（NOX2）的表达水平。结果表明，电针治疗显著改善了Aβ1-42诱导的大鼠空间学习和记忆障碍。同时，电针治疗显著恢复了AD大鼠海马区的T-AOC，并减轻了ROS、MDA和8-OH-dG水平的异常升高。更值得注意的是，电针治疗还有效改善了神经元损伤，并抵消了AD大鼠海马区NOX2水平的异常升高。我们的研究结果表明，电针是一种治疗AD的潜在策略，其可能机制与减轻神经元损伤和抑制与NOX2相关的氧化应激有关。
