title: Gastric ulcers induced by systemic hypoxia.
abstract: OBJECTIVE
  to assess the effect of systemic hypoxia on gastric mucosa and the activation of stress-responsive transcription factors induced by hypoxia.
  
  
  METHODS
  in this experimental study, rats were allocated to control and experimental groups. The experimental group was divided into subgroups and subjected to hypoxia conditions for 1, 7, 14 or 21 days. Afterwards, histopathological evaluation and study of the protein expression of the gastric mucosa were performed.
  
  
  RESULTS
  the results showed that longer exposure to hypoxic conditions leads to more severe gastric ulceration. Twenty-four hours after induction, 60% of rats had developed gastric ulcers. Seven days after induction, 80% of rats developed gastric ulcers. In the 14-day and 21-day hypoxia conditions, epithelialization (a sign of gastric ulcer healing) was observed. Evaluation of the average ulcer depth on the day of treatment showed that the greatest depth was on day 7, and the shallowest was on day 21 of treatment. Western blot analyses demonstrated that systemic hypoxia resulted in the expression of heat shock factor (HSF) and heat shock protein 70 (HSP-70), which were highest on day 7 and then regressed gradually. In control, HSF-1 and HSP-70 were not detected by Western blot analysis in the control group (normoxia).
  
  
  CONCLUSIONS
  in this study, systemic hypoxia caused gastric ulcers, and during the time of exposure to hypoxia, an adaptation process in the form of gastric epithelialization occurred in the rats. This development of gastric lesions was in line with the expression pattern of HSF-1 HIF-1 and HSP-70.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jakarta Pusat, Indonesia. ari.fahrial@ui.ac.id
authors.forename: Ari F
authors.initials: AF
authors.lastname: Syam
authors.forename: Marcellus
authors.initials: M
authors.lastname: Simadibrata
authors.forename: Septelia I
authors.initials: SI
authors.lastname: Wanandi
authors.forename: Bethy S
authors.initials: BS
authors.lastname: Hernowo
authors.forename: M
authors.initials: M
authors.lastname: Sadikin
authors.forename: Abdul A
authors.initials: AA
authors.lastname: Rani
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics*; D000818:Animals; D019610:Cytoprotection; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism / Q000503:physiopathology; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D000860:Hypoxia / Q000150:complications / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D008297:Male; D010100:Oxygen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013276:Stomach Ulcer / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D013312:Stress, Physiological / Q000235:genetics*; D013997:Time Factors; D014945:Wound Healing
chemical_list: D018840:HSP70 Heat-Shock Proteins; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D010100:Oxygen