Shi Guang-Xia, Wang Xue-Rui, Yan Chao-Qun, He Tian, Yang Jing-Wen, Zeng Xiang-Hong, Xu Qian, Zhu Wen, Du Si-Qi, Liu Cun-Zhi
Acupuncture and Moxibustion Department, Beijing Hospital of Traditional Chinese Medicine affiliated to Capital Medical University, 23 Meishuguanhou Street, Dongcheng District, Beijing 100010, China.
Sci Rep. 2015 Dec 10;5:17981. doi: 10.1038/srep17981.
In the current study, we aimed to investigate whether NADPH oxidase, a major ROS-producing enzyme, was involved in the antioxidant effect of acupuncture on cognitive impairment after cerebral ischaemia. The cognitive function, infract size, neuron cell loss, level of superoxide anion and expression of NADPH oxidase subunit in hippocampus of two-vessel occlusion (2VO) rats were determined after 2-week acupuncture. Furthermore, the cognitive function and production of O2(-) were determined in the presence and absence of NADPH oxidase agonist (TBCA) and antagonist (Apocynin). The effect of acupuncture on cognitive function after cerebral ischaemia in gp91phox-KO mice was evaluated by Morris water maze. Acupuncture reduced infarct size, attenuated overproduction of O2(-), and reversed consequential cognitive impairment and neuron cell loss in 2VO rats. The elevations of gp91phox and p47phox after 2VO were significantly decreased after acupuncture treatment. However, no differences of gp91phox mRNA were found among any experimental groups. Furthermore, these beneficial effects were reversed by TBCA, whereas apocynin mimicked the effect of acupuncture by improving cognitive function and decreasing O2(-) generation. Acupuncture failed to improve the memory impairment in gp91phox KO mice. Full function of the NADPH oxidase enzyme plays an important role in neuroprotective effects against cognitive impairment via inhibition of NAPDH oxidase-mediated oxidative stress.
在本研究中,我们旨在探究作为主要活性氧生成酶的NADPH氧化酶是否参与针刺对脑缺血后认知功能障碍的抗氧化作用。在对双动脉闭塞(2VO)大鼠进行为期2周的针刺治疗后,测定其认知功能、梗死面积、神经元细胞丢失、海马中超氧阴离子水平以及NADPH氧化酶亚基的表达。此外,在存在和不存在NADPH氧化酶激动剂(TBCA)和拮抗剂(Apocynin)的情况下,测定认知功能和超氧阴离子的产生。通过莫里斯水迷宫评估针刺对gp91phox基因敲除(KO)小鼠脑缺血后认知功能的影响。针刺可减小2VO大鼠的梗死面积,减弱超氧阴离子的过量产生,并逆转随之而来的认知功能障碍和神经元细胞丢失情况。针刺治疗后,2VO大鼠gp91phox和p47phox升高的情况显著降低。然而,在任何实验组之间均未发现gp91phox mRNA存在差异。此外,TBCA可逆转这些有益作用;而Apocynin则通过改善认知功能和减少超氧阴离子的产生来模拟针刺的作用。针刺未能改善gp91phox基因敲除小鼠的记忆障碍。NADPH氧化酶的完整功能通过抑制NAPDH氧化酶介导的氧化应激,在对认知功能障碍的神经保护作用中发挥重要作用。