Journal
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
Volume 61, Issue 5, Pages 461-469Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.etp.2008.10.010
Keywords
Catalpol; Inflammation; Mitochondria; NF-kappa B; Lipopolysaccharide
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Funding
- Key International S&T Cooperation Projects [2005DFA40790]
- National Science Foundation [20072185]
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The aim of this study was to investigate whether catalpol could facilitate recovery from lipopolysaccharide (LPS)-induced cognitive deficits and protect brain mitochondrial function from LPS-induced acute systemic inflammation. In the study, except control group, mice were challenged with a single dose of LPS (100 mu g/mouse, i.p.) to mimic an acute peripheral infection. The results showed that LPS enhanced nuclear factor kappa B (NF-kappa B) activation and induced a loss in mitochondrial integrity as shown by a significant decrease in membrane potential and increase in mitochondrial permeability transition pore opening. Pretreatment with catalpol (10 mg/kg d, i.p.) for 10 d before injection of LPS reversed the memory deficits induced by LPS, protected brain mitochondrial function, and attenuated LPS-induced NF-kappa B activation. Taken together, these data indicate that catalpol may possess therapeutic potential against LPS-induced acute systemic inflammation by attenuating NF-kappa B activation and protecting mitochondrial function in cerebral cortex and hippocampus. (C) 2008 Elsevier GmbH. All rights reserved.
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