Epimedium flavonoids ameliorate neuropathological changes and increases IGF-1 expression in C57BL/6 mice exposed to cuprizone.

Abstract	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.
Authors	Mengru Liang, Yongyan Chen, Li Zhang, Lin Li, Guangliang Chen, Linlin Yin
Journal	Neurochemical research (Neurochem Res) Vol. 40 Issue 3 Pg. 492-500 (Mar 2015) ISSN: 1573-6903 [Electronic] United States
PMID	25663299 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Chelating Agents Flavonoids Plant Extracts insulin-like growth factor-1, mouse Cuprizone Insulin-Like Growth Factor I
Topics	Animals Chelating Agents (administration & dosage) Corpus Callosum (drug effects, metabolism, pathology) Cuprizone (administration & dosage) Dose-Response Relationship, Drug Epimedium Female Flavonoids (pharmacology) Gene Expression Regulation Insulin-Like Growth Factor I (biosynthesis) Mice Mice, Inbred C57BL Plant Extracts (isolation & purification, pharmacology)

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