title: Protective effects of a phosphatidylcholine-enriched diet in lipopolysaccharide-induced experimental neuroinflammation in the rat.
abstract: Our goal was to characterize the neuroprotective properties of orally administered phosphatidylcholine (PC) in a rodent model of systemic inflammation. Sprague-Dawley rats were killed at 3 h, 1 day, 3 days, or 7 days after i.p. administration of lipopolysaccharide (LPS) to determine the plasma levels of tumor necrosis factor α (TNF-α) and interleukin 6 cytokines. The control group and one group of LPS-treated animals were nourished with standard laboratory chow, whereas another LPS-treated group received a special diet enriched with 1% PC for 5 days before the administration of LPS and thereafter during the 7-day observation period. Immunohistochemistry was performed to visualize the bromodeoxyuridine and doublecortin-positive neuroprogenitor cells and Iba1-positive microglia in the hippocampus, whereas the degree of mucosal damage was evaluated on ileal and colon biopsy samples after hematoxylin-eosin staining. The activities of proinflammatory myeloperoxidase and xanthine-oxidoreductase and the tissue nitrite/nitrate (NOx) level were additionally determined, and the cognitive functions were monitored via Morris water maze testing. The inflammatory challenge transiently increased the hippocampal NOx level and led to microglia accumulation and decreased neurogenesis. The intestinal damage, mucosal myeloperoxidase, xanthine-oxidoreductase, and NOx changes were less pronounced, and long-lasting behavioral alterations were not observed. Phosphatidylcholine pretreatment reduced the plasma TNF-α and hippocampal NOx changes and prevented the decreased neurogenesis. These data demonstrated the relative susceptibility of the brain to the consequences of transient peripheral inflammatory stimuli. Phosphatidylcholine supplementation did not reduce the overall extent of peripheral inflammatory activation, but efficiently counteracted the disturbed hippocampal neurogenesis by lowering circulating TNF-α concentrations.
authors.affiliation: Institute of Surgical Research, Department of Dermatology/Allergology, University of Szeged, Szeged, Hungary.
authors.forename: Tünde
authors.initials: T
authors.lastname: Tokés
authors.forename: Gábor
authors.initials: G
authors.lastname: Eros
authors.forename: Attila
authors.initials: A
authors.lastname: Bebes
authors.forename: Petra
authors.initials: P
authors.lastname: Hartmann
authors.forename: Szilvia
authors.initials: S
authors.lastname: Várszegi
authors.forename: Gabriella
authors.initials: G
authors.lastname: Varga
authors.forename: József
authors.initials: J
authors.lastname: Kaszaki
authors.forename: Károly
authors.initials: K
authors.lastname: Gulya
authors.forename: Miklós
authors.initials: M
authors.lastname: Ghyczy
authors.forename: Mihály
authors.initials: M
authors.lastname: Boros
mesh_terms: D000818:Animals; D000089662:Doublecortin Protein; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects* / Q000276:immunology*; D007082:Ileum / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D007150:Immunohistochemistry; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D017628:Microglia / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000276:immunology*; D009195:Peroxidase / Q000378:metabolism; D010713:Phosphatidylcholines / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013234:Stem Cells / Q000166:cytology / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014968:Xanthine Dehydrogenase / Q000378:metabolism
chemical_list: C000714848:Dcx protein, rat; D000089662:Doublecortin Protein; D008070:Lipopolysaccharides; D010713:Phosphatidylcholines; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D014968:Xanthine Dehydrogenase