Difficult Establishment of a Chronic Nonsteroidal Anti-inflammatory Drugs Induced Gastric Inflammation Rat Model due to Gastric Adaptation and Small Bowel Damage.
10.4166/kjg.2014.63.6.341
- Author:
Byoung Hwan LEE
1
;
Nayoung KIM
;
Ryoung Hee NAM
;
Ju Yup LEE
;
Hye Seung LEE
;
Chang Hee LEE
;
Ji Hyun PARK
;
Dong Ho LEE
Author Information
1. Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea. nayoungkim49@empas.com
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Adaptation;
Glucosamine;
Gastric;
Nonsteroidal anti-inflammatory agents;
Small intestine
- MeSH:
Animals;
Anti-Inflammatory Agents, Non-Steroidal/*toxicity;
Disease Models, Animal;
Gastric Mucosa/*drug effects/enzymology/pathology;
Glucosamine/metabolism;
Indomethacin/*toxicity;
Intestine, Small/*drug effects/pathology;
Male;
Peroxidase/metabolism;
Rats;
Rats, Sprague-Dawley;
Time Factors
- From:The Korean Journal of Gastroenterology
2014;63(6):341-347
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: The prevalence of peptic ulcer disease has not decreased mainly due to an increase in the use of NSAIDs. This study was conducted in order to determine whether a chronic NSAID-induced gastric inflammation model could be established by repeated administration of NSAID. METHODS: Indomethacin (10 mg/kg) was administered once per week for six weeks in 8- and 26-week rats and animals were sacrificed every week after administration. Gross ulcer index, histologic damage index, myeloperoxidase (MPO) activity, and mucus (glucosamine) levels were measured. Small bowel damage was also evaluated. RESULTS: Gross gastric damage index showed a peak level at three weeks and then decreased slowly in the 26-week indomethacin group. Gastric mucosal glucosamine level increased in both the 8-week (p=0.038) and 26-week groups (p=0.007). In addition, gastric mucosal MPO level decreased in the 8-week group (p=0.018) but did not show a decrease in the 26-week group. Small bowel damage began to occur at three weeks during the schedule and eight of 36 rats (22.2%) died due to perforation or peritonitis of the small bowel in the 8- and 26-week indomethacin groups, respectively. CONCLUSIONS: Due to gastric adaptation and small bowel damage, repeated administration of NSAID to experimental animals may not be an adequate method for establishment of the chronic gastric inflammation model.
