Electroacupuncture acutely improves cerebral blood flow and attenuates moderate ischemic injury via an endothelial mechanism in mice.
Electroacupuncture acutely improves cerebral blood flow and attenuates moderate ischemic injury via an endothelial mechanism in mice.
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DOI：
10.1371/journal.pone.0056736
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Shin HK
中科院分区：
文献类型：
--
作者：
Kim JH;Choi KH;Jang YJ;Bae SS;Shin BC;Choi BT;Shin HK
电针是一种基于传统针灸与现代电疗相结合的新型疗法，目前正被研究用于治疗急性缺血性中风。在这里，我们研究了急性EA刺激是否改善实验诱导的小鼠脑缺血后的组织和功能结果。我们假设内皮型一氧化氮合酶（eNOS）介导的灌注增强与EA干预急性缺血性损伤的有益作用有关。电针百会穴（GV 20）和大椎穴（GV 14）可增加大脑皮层的脑灌注，而eNOS KO则抑制了这一作用，但对平均动脉压（MABP）无反应。毒蕈碱型乙酰胆碱受体（mAChR）阻断剂（阿托品）可完全阻断电针引起的脑灌注增加，而β-肾上腺素能受体阻断剂（普萘洛尔）、α-肾上腺素能受体阻断剂（酚妥拉明）或烟碱型乙酰胆碱受体（nAChR）阻断剂（美加明）则不能阻断电针引起的脑灌注增加。此外，电针还可增加大脑皮层乙酰胆碱（ACh）的释放和mAChR M3的表达。与大脑中动脉闭塞（MCAO）60分钟（中度缺血性损伤）后24小时的对照组小鼠相比，闭塞后的急性EA刺激显著减少了34.5%的梗死体积，但90分钟MCAO（重度缺血性损伤）则没有。此外，在eNOS KO中，EA对中度缺血损伤的影响完全消除。与较小的梗死面积一致，急性EA刺激导致神经功能和前庭运动功能的显著改善。我们的研究结果表明，急性EA刺激后，中度局灶性脑缺血，但不严重的缺血改善组织和功能的恢复和ACh/eNOS介导的灌注增强可能与这些有益的影响EA干预急性缺血性损伤。
Electroacupuncture (EA) is a novel therapy based on traditional acupuncture combined with modern eletrotherapy that is currently being investigated as a treatment for acute ischemic stroke. Here, we studied whether acute EA stimulation improves tissue and functional outcome following experimentally induced cerebral ischemia in mice. We hypothesized that endothelial nitric oxide synthase (eNOS)-mediated perfusion augmentation was related to the beneficial effects of EA by interventions in acute ischemic injury. EA stimulation at Baihui (GV20) and Dazhui (GV14) increased cerebral perfusion in the cerebral cortex, which was suppressed in eNOS KO, but there was no mean arterial blood pressure (MABP) response. The increased perfusion elicited by EA were completely abolished by a muscarinic acetylcholine receptor (mAChR) blocker (atropine), but not a β-adrenergic receptor blocker (propranolol), an α-adrenergic receptor blocker (phentolamine), or a nicotinic acetylcholine receptor (nAChR) blocker (mecamylamine). In addition, EA increased acetylcholine (ACh) release and mAChR M3 expression in the cerebral cortex. Acute EA stimulation after occlusion significantly reduced infarct volume by 34.5% when compared to a control group of mice at 24 h after 60 min-middle cerebral artery occlusion (MCAO) (moderate ischemic injury), but not 90-min MCAO (severe ischemic injury). Furthermore, the impact of EA on moderate ischemic injury was totally abolished in eNOS KO. Consistent with a smaller infarct size, acute EA stimulation led to prominent improvement of neurological function and vestibule-motor function. Our results suggest that acute EA stimulation after moderate focal cerebral ischemia, but not severe ischemia improves tissue and functional recovery and ACh/eNOS-mediated perfusion augmentation might be related to these beneficial effects of EA by interventions in acute ischemic injury.
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影响因子：
1.9
作者：
Han, Xiaohua;Huang, Xiaolin;Chen, Hong
通讯作者：
Chen, Hong
影响因子：
1.9
作者：
Du, Yuanhao;Shi, Lei;Fan, Xiaonong
通讯作者：
Fan, Xiaonong
重复电针预处理减弱大鼠局灶性脑缺血后基质金属蛋白酶9的表达和活性
影响因子：
1.9
作者：
Dong, Hui;Fan, Yan-Hong;Xiong, Li-Ze
通讯作者：
Xiong, Li-Ze
影响因子：
5
作者：
DAUPHIN, F;HAMEL, E
通讯作者：
HAMEL, E
DOI：
10.1097/00004647-199609000-00023
发表时间：
1996-09-01
影响因子：
6.3
作者：
Huang, ZH;Huang, PL;Moskowitz, MA
通讯作者：
Moskowitz, MA