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Brain-derived neurotrophic factors increase the proliferation and differentiation of endogenous neural stem cells in mouse models of cerebral infarction

Brain-derived neurotrophic factors increase the proliferation and differentiation of endogenous neural stem cells in mouse models of cerebral infarction

作     者:Dawei Zang Juan Liu Xianhua Zuo Surindar Cheema 

作者机构:Department of Neurology Tianjin First Central Hospital Tianjin 300192 China Division of Microbiology Department of Laboratory Tianjin First Central Hospital Tianjin 300192 China Howard Florey Institute Medical College the University of Melbourne Australia 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2007年第2卷第3期

页      面:134-137页

核心收录:

学科分类:1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

主  题:stem cells brain-derived neurotrophic factor neurons mice 

摘      要:BACKGROUND: It has been confirmed that brain-derived neurotrophic factor (BDNF) can promote the proliferation of neural stem cells (NSCs) and protect neuron-like cells in vitro. However, its effect on endogenous NSCs in vivo is still unclear. OBJECTIVE: To evaluate whether BDNF can induce the endogenous NSCs to proliferate and differentiate into the neurons in the mice model of cerebral infarction. DESIGN: A synchronal controlled observation. SETTINGS: Department of Neurology, Microbiology Division of the Department of Laboratory, Tianjin First Central Hospital; Howard Florey Institute, Medical College, the University of Melbourne. MATERIALS: Twenty-four pure breed C57BL/6J mice at the age of 10 weeks old (12 males and 12 females) were divided into saline control group and BDNF-treated group, 6 males and 6 females in each group. METHODS: The experiments were performed at the University of Melbourne from July 2004 to February 2005. ① The left middle cerebral artery (MCA) was ligated in both groups to establish models of cerebral infarction and the Matsushita measuring method was used to monitor the blood flow of the lesioned region supplied by MCA. 75% reduction of blood flow should be reached in the lesioned region. ② At 24 hours after infarction, mice in the BDNF-treated group were administrated with BDNF, which was slowly delivered using an ALZET osmium pump design. BDNF was dissolved in saline at the dosage of 500 mg/kg and injected into the pump, which could release the solution consistently in the following 28 days. The mice in the saline control group accepted the same volume of saline at 24 hours after infarction. ③ The Rotarod function test began at 1 week preoperatively, the time stayed on Rotarod was recorded. The mice were tested once a day till the end of the experiment. At 4 weeks post cerebral infarction, double labeling of Nestin and GFAP, BIH tubulin and CNPase immunostaining was performed to observe the differentiation directions of the re-expressed

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