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Electroacupuncture pretreatment inhibits NADPH oxidase-mediated oxidative stress in diabetic mice with cerebral ischemia

机译:电针预处理可抑制NADPH氧化酶介导的糖尿病性脑缺血小鼠氧化应激

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摘要

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.
机译: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。给雄性C57BL / 6小鼠注射链脲佐菌素以诱发糖尿病。小鼠在“百会”穴位用EA预处理30分钟。 EA预处理结束后两小时,再灌注24小时后诱发局灶性脑缺血。在存在或不存在NADPH氧化酶抑制剂Apocynin或四溴肉桂酸活化剂(TBCA)的情况下,确定神经行为评分和梗死体积,丙二醛(MDA),活性氧(ROS)和NADPH氧化酶的活化。 EA预处理可减少糖尿病小鼠再灌注后24 h的梗塞面积并改善神经功能。与对照组相比,EA还降低了大脑的MDA和ROS水平,并抑制了NADPH氧化酶的活化。 TBCA取消了有​​益作用,而用Apocynin进行的预处理模仿了EA的神经保护和抗氧化作用。我们的结果表明,EA通过抑制NAPDH氧化酶介导的糖尿病小鼠的脑损伤来减轻脑缺血损伤。这些结果表明在糖尿病性脑缺血中EA预处理诱导的耐受性的新机制。

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