title: Pterostilbene ameliorates tumor necrosis factor alpha-induced pancreatitis in vitro.
abstract: BACKGROUND
  We have previously demonstrated that pterostilbene, a compound in blueberries, exerts antiproliferative effects against pancreatic adenocarcinoma. However, little is known about the anti-inflammatory effects of pterostilbene in pancreatitis. Therefore, the aim of this study was to evaluate the effect of pterostilbene on inflammatory markers in an in vitro pancreatitis model. We hypothesized that pterostilbene would ameliorate the immediate inflammatory response in tumor necrosis factor alpha (TNF-α)-induced pancreatitis through downregulation of signal transducer and activator of transcription 3 (STAT3) and inhibition of TNF-α-induced secretion of lipase and proinflammatory cytokines interleukins (ILs) 1β and 6.
  
  
  METHODS
  AR42J acinar cells were pretreated with TNF-α to induce pancreatitis followed by 25 and 50 μM pterostilbene for 15 and 30 min. Secretion of lipase was quantified using a lipase assay and used as a marker of TNF-α-induced pancreatitis. Detection of STAT3, IL-1β, and IL-6 was performed using enzyme-linked immunosorbent assay. Analysis of variance and Tukey post hoc analysis were used for statistical analysis.
  
  
  RESULTS
  TNF-α increased the secretion of lipase, IL-1β, and IL-6. Pterostilbene treatment inhibited TNF-α-induced secretion of lipase (P<0.01 and P<0.001), IL-1β (P<0.05), and IL-6 (P<0.05 and P<0.01). Inhibition of STAT3 by pterostilbene occurred with treatment doses of 25 and 50 μM (P<0.001 and P<0.01).
  
  
  CONCLUSIONS
  The dietary compound pterostilbene exerts an anti-inflammatory effect in pancreatitis through downregulation of STAT3 and decreased the secretion of lipase, IL-1β, and IL-6. Pterostilbene's amelioration of pancreatitis in vitro makes it an advantageous anti-inflammatory agent. Further studies are necessary to determine pterostilbene's role as a protective or therapeutic agent in pancreatitis.
authors.affiliation: Department of Surgery, Danbury Hospital, Danbury, Connecticut, USA.
authors.forename: Denise
authors.initials: D
authors.lastname: McCormack
authors.forename: Debbie
authors.initials: D
authors.lastname: McDonald
authors.forename: David
authors.initials: D
authors.lastname: McFadden
mesh_terms: D061354:Acinar Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002460:Cell Line; D004347:Drug Interactions; D066298:In Vitro Techniques; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008049:Lipase / Q000378:metabolism; D010195:Pancreatitis / Q000139:chemically induced* / Q000188:drug therapy* / Q000473:pathology; D035721:Pterocarpus / Q000737:chemistry; D051381:Rats; D050796:STAT3 Transcription Factor / Q000378:metabolism; D013267:Stilbenes / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D053583:Interleukin-1beta; D015850:Interleukin-6; D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat; D013267:Stilbenes; D014409:Tumor Necrosis Factor-alpha; C107773:pterostilbene; D008049:Lipase