title: The impact of dehydroepiandrosterone on indomethacin-induced gastric lesions in rats.
abstract: Gastric ulcer is a common gastrointestinal disease. One suggested mechanism is increased oxidative stress. Puplished data showed that dehydroepiandrosterone (DHEA) may limit oxidative stress and lipid peroxidation.
  
  
  OBJECTIVE
  To investigate the protective effect of DHEA on indomethacin-induced gastric ulcers in rats.
  
  
  METHODS
  Forty male rats were randomly divided into four groups: l)
  
  
  METHODS
  receive the vehicle, 2) DHEA-treated group, 3) Indomethacin-induced ulcer group and 4) DHEA pretreated (prior to indomethacin) group. At the end of the experiment, rats were killed and the gastric contents were collected to determine the pH and acid concentration. Gastric mucosa was examined macroscopically and then parts of the tissues were collected for histopathological examination. Other parts of the gastric mucosa were homogenized to measure the levels of lipid peroxidation and oxidative stress parameters.
  
  
  RESULTS
  Indomethacin-treated rats showed increased gastric acidity, acid concentration and ulcer index as compared to control rats. This is confirmed by histopathological studies. DHEA pre-treatment proir to indomethacin administration ameliorated all changes seen in the ulcered group.
  
  
  CONCLUSIONS
  DHEA has a protective effect against indomethacin-induced gastric ulcers through decreasing acid secretion, prevention of lipid peroxidation and improving endogenous gastric antioxidant system.
authors.affiliation: College of Health Sciences Paaet Kuwait.
authors.forename: S
authors.initials: S
authors.lastname: Eleawa
authors.affiliation: King Khalid University Department of Physiology, College of Medicine Abha Kingdom of Saudi Arabia.
authors.forename: I
authors.initials: I
authors.lastname: Bin-Jaliah
authors.affiliation: King Khalid University Department of Physiology, College of Medicine Abha Kingdom of Saudi Arabia.
authors.forename: M
authors.initials: M
authors.lastname: Alkhateeb
authors.affiliation: King Saud University Department of Physiology, College of Medicine Riyadh Saudi Arabia.
authors.forename: N M K
authors.initials: NM
authors.lastname: Bayoumy
authors.affiliation: King Khalid University Department of Biochemistry, College of Medicine Abha Saudi Arabia.
authors.forename: R
authors.initials: R
authors.lastname: Alessa
authors.affiliation: King Khalid University Department of Physiology, College of Medicine Abha Kingdom of Saudi Arabia Mansoura University Department of Medical Physiology, College of Medicine PO Box: 35516 Mansoura Egypt.
authors.forename: Hussein F
authors.initials: HF
authors.lastname: Sakr
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D019610:Cytoprotection; D003687:Dehydroepiandrosterone / Q000494:pharmacology*; D004195:Disease Models, Animal; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007213:Indomethacin; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013276:Stomach Ulcer / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D003687:Dehydroepiandrosterone; D002374:Catalase; D013482:Superoxide Dismutase; D007213:Indomethacin
keywords: DHEA; gastric ulcer; indomethacin; inflammation; oxidative stress