Electroacupuncture pretreatment inhibits NADPH oxidase-mediated oxidative stress in diabetic mice with cerebral ischemia
Electroacupuncture pretreatment inhibits NADPH oxidase-mediated oxidative stress in diabetic mice with cerebral ischemia
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DOI：
10.1016/j.brainres.2014.05.020
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发表时间：
2014-07-21
期刊：
影响因子：
2.9
通讯作者：
Xiong, Lize
中科院分区：
文献类型：
--
作者：
Guo, Fan;Song, Wenying;Xiong, Lize
我们研究了电针（EA）对糖尿病小鼠脑缺血损伤的保护作用，并探讨了NADPH氧化酶介导的氧化应激的作用。雄性 C57BL/6 小鼠注射链脲佐菌素诱导糖尿病。小鼠用电针预处理“百会”穴30 min。 EA预处理结束后2小时，24小时再灌注后诱发局灶性脑缺血。在存在或不存在 NADPH 氧化酶抑制剂罗布麻素或激活剂四溴肉桂酸 (TBCA) 的情况下测定神经行为评分和梗死体积、丙二醛 (MDA)、活性氧 (ROS) 和 NADPH 氧化酶的激活。 EA 预处理可减少糖尿病小鼠再灌注 24 小时后的梗塞面积并改善神经系统结果。与对照组相比，电针还降低了脑内MDA和ROS水平，并抑制了NADPH氧化酶的激活。 TBCA 消除了有益作用，而罗布麻素预处理模仿了 EA 的神经保护和抗氧化作用。我们的结果表明，EA 通过抑制糖尿病小鼠 NAPDH 氧化酶介导的氧化损伤来减轻脑缺血损伤。这些结果表明 EA 预处理诱导糖尿病脑缺血耐受的新机制。 (C) 2014 Elsevier B.V. 保留所有权利。
We investigated the protective effect of electroacupuncture (EA) on cerebral ischemic injury in diabetic mice, and explored the role of NADPH oxidase-mediated oxidative stress. Male C57BL/6 mice were injected streptozotocin to induce diabetes. The mice were pretreated with EA at acupoint "Baihui" for 30 min. Two hours after the end of EA pretreatment, focal cerebral ischemia was induced following 24 h reperfusion. The neurobehavioral scores and infarction volumes, malondialdehyde (MDA), reactive oxygen species (ROS), and activation of NADPH oxidase were determined in the presence or absence of the NADPH oxidase inhibitor apocynin or activator tetrabromocinnamic acid (TBCA). EA pretreatment reduced infarct size and improved neurological outcomes 24 h after reperfusion in the diabetic mice. EA also decreased cerebral MDA and ROS levels compared with the control group, and inhibited the NADPH oxidase activation. The beneficial effects were abolished by TBCA while pretreatment with apocynin mimicked the neuroprotective and anti-oxidative effects of EA. Our results demonstrated that EA attenuated cerebral ischemic injury by inhibiting NAPDH oxidase-mediated oxidative damage in diabetic mice. These results suggest a novel mechanism of EA pretreatment-induced tolerance in diabetic cerebral ischemia. (C) 2014 Elsevier B.V. All rights reserved.