ArticleNeurochemistry international2010
Rat brain docosahexaenoic acid metabolism is not altered by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide.
Article in Neurochemistry international, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Compound-Specific Isotope Analysis as a Potential Approach for Investigation of Cerebral Accumulation of Docosahexaenoic Acid: Previous Milestones and Recent Trends.Molecular neurobiology · 2025Review
- Age-Related Changes in the Gut Microbiota Modify Brain Lipid Composition.Frontiers in cellular and infection microbiology · 2019Article
- Dietary Linoleic Acid Lowering Reduces Lipopolysaccharide-Induced Increase in Brain Arachidonic Acid Metabolism.Molecular neurobiology · 2017Article
- Dose-dependent changes in neuroinflammatory and arachidonic acid cascade markers with synaptic marker loss in rat lipopolysaccharide infusion model of neuroinflammation.BMC neuroscience · 2012Article
- Imaging brain signal transduction and metabolism via arachidonic and docosahexaenoic acid in animals and humans.Brain research bulletin · 2012Review
- Acetate supplementation attenuates lipopolysaccharide-induced neuroinflammation.Journal of neurochemistry · 2011Article
- Lithium modifies brain arachidonic and docosahexaenoic metabolism in rat lipopolysaccharide model of neuroinflammation.Journal of lipid research · 2010Article
- Bacterial lipopolysaccharide induces a dose-dependent activation of neuroglia and loss of basal forebrain cholinergic cells in the rat brain.Inflammation and cell signalingArticle
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
In a rat model of neuroinflammation, produced by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide (LPS), we reported that the brain concentrations of non-esterified brain arachidonic acid (AA, 20:4 n-6) and its eicosanoid products PGE(2) and PGD(2) were increased, as were AA turnover rates in certain brain phospholipids and the activity of AA-selective cytosolic phospholipase A(2) (cPLA(2)). The activity of Ca(2+)-independent iPLA(2), which is thought to be selective for the release of docosahexaenoic acid (DHA, 22:6 n-3) from membrane phospholipid, was unchanged. In the present study, we measured parameters of brain DHA metabolism in comparable artificial cerebrospinal fluid (control) and LPS-infused rats. In contrast to the reported changes in markers of AA metabolism, the brain non-esterified DHA concentration and DHA turnover rates in individual phospholipids were not significantly altered by LPS infusion. The formation rates of AA-CoA and DHA-CoA in a microsomal brain fraction were also unaltered by the LPS infusion. These observations indicate that LPS-treatment upregulates markers of brain AA but not DHA metabolism. All of which are consistent with other evidence that suggest different sets of enzymes regulate AA and DHA recycling within brain phospholipids and that only selective increases in brain AA metabolism occur following a 6-day LPS infusion.
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