Journal
NEUROBIOLOGY OF LEARNING AND MEMORY
Volume 96, Issue 2, Pages 156-165Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nlm.2011.03.010
Keywords
LPS; Inflammatory response; Ursolic acid; P38/NF-kappa B pathways; Cognitive deficits
Funding
- Jiangsu Higher Education Institutions (PAPD)
- Scientific and Technological Innovation Team of Jiangsu College and University
- Natural Science Foundation for Colleges and Universities in Jiangsu Province [09KJB180009]
- National Natural Science Foundation of China [30950031]
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China [07KJA36029]
- Key Laboratory of Jiangsu Province, PR China
- Natural Science Foundation by Xuzhou Normal University [08XLR09, 09XLY05, 09XKXK02]
- Xuzhou Normal University [08YLA007]
- postgraduate innovation projects of Jiangsu Province
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Evidence indicates that systemic administration of lipopolysaccharide (LPS) induces brain inflammation, ultimately resulting in cognitive deficits. Ursolic acid (UA), a plant-derived pentacyclic triterpenoid, is well known to possess multiple biological functions, including antioxidant, anti-tumor and anti-inflammatory activities. In the present study, we assessed the protective effect of UA against the LPS-induced cognitive deficits in mice. We found that UA significantly improved cognitive deficits of LPS-treated mice in open field, step-through passive avoidance and Morris water maze tasks. One potential mechanism of this action was attributed to the decreased production of pro-inflammatory markers including COX-2, iNOS, TNE-alpha, IL-1 beta, IL-2 and IL-6 in LPS-treated mouse brain. Mechanistically, UA markedly inhibited LPS-induced I kappa B alpha phosphorylation and degradation, NF-kappa B p65 nuclear translocation and p38 activation in mouse brain, but did not affect the activation of TLR4, MyD88, ERK, JNK and Akt. Taken together, these results suggest that UA may be useful for mitigating inflammation-associated brain disorders by inhibiting pro-inflammatory factors production, at least in part, through blocking the p38/NF-kappa B signaling pathways. Crown Copyright (C) 2011 Published by Elsevier Inc. All rights reserved.
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