title: Administration of obestatin accelerates the healing of chronic gastric ulcers in rats.
abstract: BACKGROUND
  Previous studies have shown that administration of obestatin exhibits a protective effect in the pancreas, attenuating the development of acute pancreatitis. The aim of the present study was to investigate the influence of obestatin administration on the healing of chronic gastric ulcers.
  
  
  METHODS
  Chronic gastric ulcers were induced in rats by 100% acetic acid applied to the serosal surface of the gastric wall. Obestatin was given twice a day intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose for 6 days. Six days after induction of ulcers, rats were anesthetized and the stomach was exposed for measurement of gastric blood flow and ulcer area. Biopsy samples from the gastric mucosa were taken for determination of mucosal DNA synthesis and for measurement of gastric expression of mRNA for interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).
  
  
  RESULTS
  Induction of gastric ulcers alone increased mucosal blood flow and tissue expression of mRNA for TNF-alpha and IL-1beta, whereas gastric mucosal DNA synthesis was reduced. In rats with gastric ulcers, administration of obestatin increased gastric mucosal blood flow, accelerated the healing rate of these ulcers and partly reversed the gastric ulcer-induced reduction in gastric mucosal DNA synthesis. These results were associated with a reduction in gastric mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.
  
  
  CONCLUSIONS
  Treatment with obestatin increases gastric mucosal blood flow and cell proliferation, leading to acceleration of healing of gastric ulcers. These effects are associated with a reduction in mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.
authors.affiliation: Department of Physiology, Jagiellonian University Medical College, Cracow, Poland. mpdembin@cyf-kr.edu.pl
authors.forename: Artur
authors.initials: A
authors.lastname: Dembiński
authors.forename: Zygmunt
authors.initials: Z
authors.lastname: Warzecha
authors.forename: Piotr
authors.initials: P
authors.lastname: Ceranowicz
authors.forename: Jakub
authors.initials: J
authors.lastname: Cieszkowski
authors.forename: Marcin
authors.initials: M
authors.lastname: Dembiński
authors.forename: Agata
authors.initials: A
authors.lastname: Ptak-Belowska
authors.forename: Atsukasu
authors.initials: A
authors.lastname: Kuwahara
authors.forename: Ikuo
authors.initials: I
authors.lastname: Kato
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D002908:Chronic Disease / Q000188:drug therapy*; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D054439:Ghrelin / Q000494:pharmacology* / Q000627:therapeutic use*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow; D012965:Sodium Chloride / Q000494:pharmacology; D013276:Stomach Ulcer / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D054439:Ghrelin; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D012965:Sodium Chloride