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Cell proliferation in the gastric epithelium of the ulcer rat.

Helander, Herbert F, 1935- (författare)
Göteborgs universitet, Institutionen för de kirurgiska disciplinerna, Avdelningen för gastroforskning, Gothenburg University, Institute of Surgical Sciences, Department of Gastro Research
Li, H (författare)
Göteborgs universitet Sahlgrenska akademin. Institutionen för de kirurgiska disciplinerna, Avdelningen för gastroforskning. 
2005
Engelska.
Ingår i: Scandinavian journal of gastroenterology. - 0036-5521. ; 40:12, s. 1386-93
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • OBJECTIVE: Cell division is brisk in the ulcer margin and many of the new cells will migrate over and cover the ulcer bed. The aim of this study was to determine how agents that promote or delay gastric ulcer healing influence cell proliferation in the gastric epithelium. MATERIAL AND METHODS: Acetic acid ulcers were produced in the rat gastric corpus; non-ulcer rats served as controls. All rats were given a continuous infusion of (3)H-thymidine. Some rats were also given gastrin or indomethacin, or infected with Helicobacter pylori. The rats were killed after 1, 2, 6 or 13 days, and the ulcer margin and undamaged corpus were excised for determination of labeling index (LI) by autoradiography. Antrum, duodenum and colon were also studied. Silver grain counting was carried out in some groups. RESULTS: LI in the ulcer margin grew exponentially, reaching 84% after 6 days; gastrin increased, and indomethacin decreased LI significantly. In 6-day ulcer rats that were given 3H-thymidine only during the first day LI was 5%, while in those given 3H-thymidine only during the last day LI was 27%. LI and silver grain counting results indicated that during the first 6 days of healing the epithelial cells in the ulcer margin divide twice. In the undamaged epithelium of the 1-day ulcer rats LI was <one-third, and in the antral epithelium one-half of that in the non-ulcer controls. CONCLUSIONS: During the first 6 days of healing, the LI of the non-parietal epithelial cells increases exponentially in the ulcer margin; this is enhanced by gastrin. The unexpected finding in the ulcer rats of decreased LI in undamaged oxyntic and antral epithelium may be caused by a block of the G1 restriction point in the cell cycle. The reason for this remains obscure.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  (hsv//swe)
MEDICAL AND HEALTH SCIENCES  (hsv//eng)

Nyckelord

Acetic Acid
Animals
Anti-Inflammatory Agents
Non-Steroidal
pharmacology
Cell Proliferation
drug effects
Epithelial Cells
drug effects
physiology
Female
Gastric Mucosa
drug effects
pathology
physiopathology
Gastrins
physiology
Helicobacter Infections
complications
Indomethacin
pharmacology
Rats
Rats
Sprague-Dawley
Stomach Ulcer
chemically induced
pathology
physiopathology
Thymidine
analogs & derivatives
pharmacology
Wound Healing
drug effects
physiology

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Li, H
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