Department of Nuclear Medicine, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China ; Department of Traditional Chinese Medicine & Rehabilitation, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China ; Zhejiang University Medical PET Center, Hangzhou, Zhejiang 310009, China ; Institute of Nuclear Medicine and Molecular Imaging of Zhejiang University, Hangzhou, Zhejiang 310009, China ; Key Laboratory of Medical Molecular Imaging of Zhejiang Province, Hangzhou, Zhejiang 310009, China.
Evid Based Complement Alternat Med. 2013;2013:507091. doi: 10.1155/2013/507091. Epub 2013 May 2.
Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of (18)F-fluorodeoxyglucose ((18)F-FDG) micro positron emission tomography (microPET). Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit scores, and cerebral glucose metabolism were evaluated. Levels of vascular density factor (vWF), glial marker (GFAP), and mature neuronal marker (NeuN) were assessed by immunohistochemistry. Results. The neurological deficit scores were significantly decreased in the Scu-50 group compared to the CIRU group (P < 0.001). (18)F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group (P < 0.01) and Scu-25 group (P < 0.01). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation. Conclusion. (18)F-FDG microPET imaging demonstrated metabolic recovery after Scu-50 treatment in the rat model of cerebral ischemia. The neuroprotective effects of Scu on cerebral ischemic injury might be associated with increased regional glucose activity and neuronal maturation.
目的。使用（18）F-氟脱氧葡萄糖（（18）F-FDG）微正电子发射断层扫描（microPET）研究灯盏乙素（Scu）在大鼠脑缺血模型中的神经保护作用。
方法。采用大脑中动脉闭塞法建立脑缺血模型。将大鼠分为 5 组：假手术组、脑缺血再灌注未治疗组（CIRU 组）、Scu-25 组（Scu 25mg/kg/d）、Scu-50 组（Scu 50mg/kg/d）和尼莫地平组（10mg/kg/d）。治疗组连续给药 2 周。通过评估脑梗死体积、神经功能缺损评分和脑葡萄糖代谢，评价治疗效果。通过免疫组织化学评估血管密度因子（vWF）、神经胶质标志物（GFAP）和成熟神经元标志物（NeuN）的水平。
结果。与 CIRU 组相比，Scu-50 组的神经功能缺损评分显著降低（P < 0.001）。与 CIRU 组和 Scu-25 组相比，Scu-50 组的（18）F-FDG 在同侧脑梗死区的摄取随时间推移而持续增加（P < 0.01）。免疫组织化学分析表明，Scu-50 增强了神经元的成熟。
结论。（18）F-FDG microPET 成像显示，在脑缺血大鼠模型中，Scu-50 治疗后代谢得到恢复。Scu 对脑缺血损伤的神经保护作用可能与局部葡萄糖活性增加和神经元成熟有关。
