title: Effects of sesamin-supplemented dietary fat emulsions on the ex vivo production of lipopolysaccharide-induced prostanoids and tumor necrosis factor alpha in rats.
abstract: BACKGROUND
  Sesamin, a nonfat constituent of sesame oil, inhibits Delta(5)-desaturase activity, resulting in accumulation of dihomo-gamma-linolenic acid (DGLA), which displaces arachidonic acid (AA) and consequently decreases the formation of proinflammatory 2-series prostaglandins.
  
  
  OBJECTIVE
  We sought to determine whether dietary supplementation with sesamin augments the antiinflammatory effects of dietary linseed oil in rats.
  
  
  METHODS
  We investigated the effects of continuous tube feedings of emulsions containing safflower oil or linseed oil with sesamin (SO+ and LO+) or without sesamin (SO and LO) on liver fatty acid composition and on endotoxin-induced production of prostaglandin E(2), 6-keto-prostaglandin F(1alpha), and tumor necrosis factor alpha (TNF-alpha) by whole blood from rats (n = 6 per diet group).
  
  
  RESULTS
  We found a significant accumulation of DGLA only in the liver phospholipids of animals fed SO+ and LO+ (1.8 +/- 0.2 and 1.4 +/- 0.3 mol%, respectively), which suggests that sesamin inhibited Delta(5)-desaturation of n-6 fatty acids. These changes were associated with significant reductions in plasma prostaglandin E(2) concentrations in animals fed SO+ compared with those fed SO (P: < 0. 05). Despite a significant reduction in tissue AA content in the LO group, the prostaglandin E(2) concentrations did not differ significantly from those of the SO group. Plasma concentrations of TNF-alpha were significantly lower (P: < 0.05) in the animals fed LO+ than in those fed SO (199 +/- 48 and 488 +/- 121 ng/L, respectively).
  
  
  CONCLUSIONS
  These data indicate that in rats, tube feedings of diets containing sesamin exerted antiinflammatory effects that were augmented by concurrent consumption of linseed oil.
authors.affiliation: Department of Surgery, Harvard Institutes of Medicine, Boston, MA 02218, USA.
authors.forename: T
authors.initials: T
authors.lastname: Utsunomiya
authors.forename: S R
authors.initials: SR
authors.lastname: Chavali
authors.forename: W W
authors.initials: WW
authors.lastname: Zhong
authors.forename: R A
authors.initials: RA
authors.lastname: Forse
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D004041:Dietary Fats / Q000494:pharmacology*; D019587:Dietary Supplements; D015232:Dinoprostone / Q000096:biosynthesis; D004149:Dioxoles / Q000494:pharmacology*; D004655:Emulsions; D005227:Fatty Acids / Q000378:metabolism; D017705:Lignans / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000378:metabolism; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
chemical_list: D000893:Anti-Inflammatory Agents; D004041:Dietary Fats; D004149:Dioxoles; D004655:Emulsions; D005227:Fatty Acids; D017705:Lignans; D008070:Lipopolysaccharides; D011453:Prostaglandins; D014409:Tumor Necrosis Factor-alpha; D015121:6-Ketoprostaglandin F1 alpha; D015232:Dinoprostone; C054125:sesamin