title: Effects of growth factors on aspirin-induced inhibition of wound repair in a rabbit gastric epithelial cell model.
abstract: BACKGROUND
  Aspirin is known to cause adverse effects, including gastric mucosal injury, and to retard gastric wound healing. Growth factors including hepatocyte growth factor (HGF), epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) have been shown to play an important role in the repair of gastric mucosal injury.
  
  
  OBJECTIVE
  To employ the cultured gastric epithelial cell model to elucidate the effects of aspirin, as well as several growth factors (HGF, EGF and IGF-I), on gastric wound repair.
  
  
  METHODS
  Isolated rabbit gastric epithelial cells (92% mucous cells) were cultured in F-12 medium and formed a complete monolayer cell sheet in 48 h. A wound with a cell-free area of constant size (2 mm2) was then created and the wound repair process was monitored by measuring wound size every 12 h. Proliferating cells were detected by BrdU staining. Effects of aspirin (8 mM), HGF (10 ng/mL), EGF (10 ng/mL) and IGF-I (30 ng/mL) were assessed.
  
  
  RESULTS
  Aspirin significantly retarded wound healing, but simultaneous addition of growth factors significantly accelerated wound repair compared with aspirin alone. Growth factors reversed the aspirin-induced inhibition of cell proliferation.
  
  
  CONCLUSIONS
  Growth factors, including HGF, EGF and IGF-I, reversed the aspirin-induced inhibition of wound repair through their cytoprotective effects on gastric epithelial cells.
authors.affiliation: Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshizawa
authors.forename: S
authors.initials: S
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Hirose
authors.forename: J
authors.initials: J
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Osada
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Oide
authors.forename: T
authors.initials: T
authors.lastname: Kitamura
authors.forename: Y
authors.initials: Y
authors.lastname: Takei
authors.forename: T
authors.initials: T
authors.lastname: Ogihara
authors.forename: H
authors.initials: H
authors.lastname: Miwa
authors.forename: A
authors.initials: A
authors.lastname: Miyazaki
authors.forename: N
authors.initials: N
authors.lastname: Sato
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000494:pharmacology; D001241:Aspirin / Q000009:adverse effects* / Q000494:pharmacology; D018929:Cell Culture Techniques; D002455:Cell Division / Q000187:drug effects; D019610:Cytoprotection; D004815:Epidermal Growth Factor / Q000494:pharmacology*; D004847:Epithelial Cells / Q000502:physiology*; D005753:Gastric Mucosa / Q000473:pathology*; D017228:Hepatocyte Growth Factor / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D011817:Rabbits
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D004815:Epidermal Growth Factor; D017228:Hepatocyte Growth Factor; D007334:Insulin-Like Growth Factor I; D001241:Aspirin