Table_1_Non-pulsed Sinusoidal Electromagnetic Field Rescues Animals From Severe Ischemic Stroke via NO Activation.docx

Despite the high prevalence and devastating outcome, only a few treatment options for cerebral ischemic stroke exist. Based on the nitric oxide (NO)-stimulating capacity of Non-pulsed Sinusoidal Electromagnetic Field (NP-SEMF) and the possible neuroprotective role of NO in ischemic stroke, we hypothesized that NP-SEMF is able to enhance survival and neurological outcome in a rat model of cerebral ischemia. The animals, in which ischemic injury was induced by occlusion of both common carotid arteries, received 20 min of NP-SEMF of either 10 or 60 Hz daily for 4 days. NP-SEMF dramatically increased survival, reduced the size of the infarcted brain area and significantly improved the neurological score of the surviving rats. Corresponding to previous reports, NP-SEMF was able to induce NO production in vitro. The importance of NO as a key signaling molecule was highlighted by inhibition of the NP-SEMF beneficial effects in the rat stroke model after blocking NO synthase (NOS). Our results indicate for the first time that NP-SEMF exposure (13.5 mT at 60 and 10 Hz) improves the survival and neurological outcome of rats subjected to cerebral ischemia and that this effect is mediated by NO, underlining the great therapeutic potential of NP-SEMF as a therapy for ischemic stroke.

尽管缺血性脑卒中（cerebral ischemic stroke）发病率居高不下且预后极差，当前可用的治疗方案却极为有限。基于非脉冲正弦电磁场（Non-pulsed Sinusoidal Electromagnetic Field，NP-SEMF）的一氧化氮（nitric oxide，NO）刺激特性，以及一氧化氮在缺血性脑卒中中潜在的神经保护作用，本研究提出假设：非脉冲正弦电磁场可改善大鼠脑缺血模型的存活率与神经功能预后。本研究通过结扎双侧颈总动脉构建脑缺血损伤模型，随后每日对模型大鼠施加10 Hz或60 Hz的非脉冲正弦电磁场干预，每次持续20分钟，共干预4天。结果显示，非脉冲正弦电磁场可显著提升大鼠存活率、缩小脑梗死体积，并显著改善存活大鼠的神经功能评分。与既往研究报道一致，非脉冲正弦电磁场在体外可诱导一氧化氮的产生。通过阻断一氧化氮合酶（nitric oxide synthase，NOS）可抑制非脉冲正弦电磁场的上述保护效应，这一结果也凸显了一氧化氮作为关键信号分子的重要作用。本研究首次证实，施加场强为13.5 mT的10 Hz与60 Hz非脉冲正弦电磁场干预，可改善脑缺血大鼠的存活率与神经功能预后，且该效应由一氧化氮介导，这凸显了非脉冲正弦电磁场作为缺血性脑卒中治疗手段的巨大应用潜力。