Effects of catalpol on mitochondrial function and working memory in mice after lipopolysaccharide-induced acute systemic inflammation.

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 microg/mouse, i.p.) to mimic an acute peripheral infection. The results showed that LPS enhanced nuclear factor kappa B (NF-kappaB) 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 10d before injection of LPS reversed the memory deficits induced by LPS, protected brain mitochondrial function, and attenuated LPS-induced NF-kappaB activation. Taken together, these data indicate that catalpol may possess therapeutic potential against LPS-induced acute systemic inflammation by attenuating NF-kappaB activation and protecting mitochondrial function in cerebral cortex and hippocampus.

• Authors: Aihong Zhang, Shuang Hao, Jing Bi, Yongming Bao, Xiuli Zhang, Lijia An, Bo Jiang
• Journal: Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie (Exp Toxicol Pathol) Vol. 61 Issue 5 Pg. 461-9 (Sep 2009) ISSN: 1618-1433 [Electronic] Germany
• PMID: 19081713 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents
• Glucosides
• Iridoid Glucosides
• Iridoids
• Lipopolysaccharides
• NF-kappa B
• catalpol

Topics

• Animals
• Anti-Inflammatory Agents (pharmacology)
• Brain (drug effects, metabolism)
• Glucosides (pharmacology)
• Inflammation (chemically induced)
• Iridoid Glucosides
• Iridoids (pharmacology)
• Lipopolysaccharides (toxicity)
• Maze Learning (drug effects)
• Memory (drug effects)
• Mice
• Mitochondria (drug effects)
• NF-kappa B (drug effects)