期刊
NEUROCHEMICAL RESEARCH
卷 40, 期 3, 页码 492-500出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-014-1490-0
关键词
Cuprizone; Epimedium flavonoids; Neuropathological change; Multiple sclerosis
资金
- National Natural Science Foundation of China [81001656, 81341088]
- Beijing Nova Star Program in Science and Technology [Z12111000250000]
- Capital Medical Development Special Program [2011-1001-06]
- Beijing Organization Department of the Municipal Party Committee Project for Highly Talented Men [2012D005018000010]
The cuprizone (CPZ)-induced toxic demyelinating model, characterized by the degeneration of oligodendrocytes, has been utilized to study multiple sclerosis-related lesions. The present study was designed to determine the effect of epimedium flavonoids (EF), the main component extracted from Epimedium sagittatum, on CPZ-induced neuropathological changes in the corpus callosum of C57BL/6 mice. Once we determined an EF-based protective effect on the corpus callosum, we sought to explore the underlying mechanism of this protection. To induce demyelination, 8-week-old mice were fed with 0.2 % CPZ for a maximum period of 6 weeks. EF treatment for a period of 3 weeks effectively decreased the breakdown of myelin, OL loss, and oligodendrocyte precursor cell accumulation in CPZ-fed mice. In addition, EF administration significantly increased the cortical expression level of insulin-like growth factor 1 (IGF-1). This study provides the first in vivo evidence of EF-based protection against CPZ-induced neuropathological changes. Furthermore, our study suggests that upregulated IGF-1 may play a role in this protection.
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