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论文类型：期刊论文

发表时间：2009-09-01

发表刊物：EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY

收录刊物：SCIE、PubMed、Scopus

卷号：61

期号：5

页面范围：461-469

ISSN号：0940-2993

关键字：Catalpol; Inflammation; Mitochondria; NF-kappa B; Lipopolysaccharide

摘要：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.