期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 25, 期 8, 页码 1658-1667出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2011.06.009
关键词
Ursolic acid; High-fat diet; Endoplasmic reticulum stress; I kappa B kinase beta/nuclear factor-kappa B-mediated inflammation; Insulin signaling; Cognitive impairments
资金
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Jiangsu College and University
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China [07KJA36029]
- Natural Science Foundation for Colleges and Universities in Jiangsu Province [09KJB180009]
- Key Laboratory of Jiangsu Province, PR, China
- Natural Science Foundation of Xuzhou Normal University [08XLR09, 09XLY05, 09XKXK02]
Evidence suggests that obesity-induced cognitive impairments are driven by in brain inflammatory responses and inflammation-mediated brain insulin resistance. Ursolic acid (UA), a triterpenoid compound, has many important biological functions, including antioxidant and anti-inflammatory activities. Here, we evaluated the effect of UA on cognitive impairment induced by a high-fat diet (HFD), and we explored the potential mechanisms mediating this effect. Results showed that UA administration significantly improved the behavioral performance of C57/BL6J mice fed a HFD in both the step-through test and the Morris water maze task. These results were associated with the inhibition of endoplasmic reticulum stress and I kappa B kinase beta/nuclear factor-kappa B-mediated inflammatory signaling and the restoration of insulin signaling and phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. UA administration also increased memory-related protein expression in the hippocampus of mice given a HFD. However, the neuroprotective effects of UA were blocked by an intracerebroventricular (i.c.v.) injection of PI-103, a specific PI3K 110 alpha inhibitor. These results suggest that UA may be a potent candidate for the prevention and treatment of cognitive deficits caused by type 2 diabetes. Crown Copyright (C) 2011 Published by Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据