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Indexed by:Journal Papers

Date of Publication:2009-09-01

Journal:EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY

Included Journals:SCIE、PubMed、Scopus

Volume:61

Issue:5

Page Number:461-469

ISSN No.:0940-2993

Key Words:Catalpol; Inflammation; Mitochondria; NF-kappa B; Lipopolysaccharide

Abstract: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.