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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 507091, 9 pages
Research Article

Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with 18F-Fluorodeoxyglucose MicroPET

Jin-hui Li,1,2,3,4,5 Jing Lu,6 and Hong Zhang1,3,4,5

1Department of Nuclear Medicine, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China
2Department of Traditional Chinese Medicine & Rehabilitation, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China
3Zhejiang University Medical PET Center, Hangzhou, Zhejiang 310009, China
4Institute of Nuclear Medicine and Molecular Imaging of Zhejiang University, Hangzhou, Zhejiang 310009, China
5Key Laboratory of Medical Molecular Imaging of Zhejiang Province, Hangzhou, Zhejiang 310009, China
6Department of Neurobiology, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China

Received 28 February 2013; Accepted 12 April 2013

Academic Editor: Mei Tian

Copyright © 2013 Jin-hui Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of 18F-fluorodeoxyglucose (18F-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 ( ). 18F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group ( ) and Scu-25 group ( ). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation. Conclusion. 18F-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.