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首页> 外文期刊>Scientific reports. >Acupuncture elicits neuroprotective effect by inhibiting NAPDH oxidase-mediated reactive oxygen species production in cerebral ischaemia
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Acupuncture elicits neuroprotective effect by inhibiting NAPDH oxidase-mediated reactive oxygen species production in cerebral ischaemia

机译:针刺通过抑制脑缺血中NAPDH氧化酶介导的活性氧的产生而引起神经保护作用

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摘要

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.
机译:在当前的研究中,我们旨在调查NADPH氧化酶(一种主要的ROS产生酶)是否参与针刺对脑缺血后认知障碍的抗氧化作用。针刺2周后,测定2只闭塞(2VO)大鼠海马的认知功能,侵害大小,神经元细胞丢失,超氧阴离子水平和NADPH氧化酶亚单位的表达。此外,在是否存在NADPH氧化酶激动剂(TBCA)和拮抗剂(Apocynin)的情况下,确定O 2 的认知功能和产生。莫里斯水迷宫评估了针刺对gp91phox-KO小鼠脑缺血后认知功能的影响。针刺可减少2VO大鼠的梗死面积,减轻O 2 的过度生产,并逆转相应的认知障碍和神经元细胞损失。针刺治疗后2VO后gp91phox和p47phox的升高明显降低。但是,在任何实验组之间均未发现gp91phox mRNA的差异。此外,TBCA逆转了这些有益作用,而阿朴西宁则通过改善认知功能和减少O 2 产生来模仿针刺的作用。针刺不能改善gp91phox KO小鼠的记忆力损害。 NADPH氧化酶的全部功能通过抑制NAPDH氧化酶介导的氧化应激在对抗认知障碍的神经保护作用中起重要作用。

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