Department of Pediatrics, Chinese PLA General Hospital (No. 301 Hospital of PLA), 28, Fuxing Road, Beijing 100852, China.
Brain Res. 2011 Apr 6;1383:324-8. doi: 10.1016/j.brainres.2011.01.088. Epub 2011 Jan 31.
The present study investigated the role of neuronal nitric oxide synthase (nNOS)/nitric oxide (NO) system in the pathophysiologic regulation of hypoxic-ischemic brain damage (HIBD) in baby rats subjected to electrical stimulation (ES). The motor function, NO concentration in cortex, and protein expressions of nNOS were examined after 14 sessions of ES. Results showed that NO levels in cortex significantly increased 24h after hypoxia-ischemia than sham. ES could improve motor functions in HIBD rats and spontaneously decrease nNOS/NO system. In conclusion, the nNOS/NO pathway might play a critical role as mediator of neuronal recovery in HIBD rats after undergoing ES treatment.
本研究探讨了电刺激（ES）作用下，神经元型一氧化氮合酶（nNOS）/一氧化氮（NO）系统在新生大鼠缺氧缺血性脑损伤（HIBD）病理生理调节中的作用。电刺激 14 次后，检测了大鼠的运动功能、皮质中 NO 浓度和 nNOS 的蛋白表达。结果显示，缺氧缺血后 24 小时，皮质中 NO 水平明显高于假手术组。电刺激可改善 HIBD 大鼠的运动功能，并自发降低 nNOS/NO 系统。综上所述，nNOS/NO 通路可能在 HIBD 大鼠接受电刺激治疗后，作为神经元恢复的中介物发挥关键作用。
