TY - JOUR
T1 - Is omeprazole or misoprostol superior for improving indomethacin-lnduced delayed maturation of granulation tissue in rat gastric ulcers?
AU - Arisawa, Tomiyasu
AU - Harata, Masao
AU - Kamiya, Yoshio
AU - Shibata, Tomoyuki
AU - Nagasaka, Mitsuo
AU - Nakamura, Masakatsu
AU - Fujita, Hiroshi
AU - Hasegawa, Shin
AU - Nakamura, Masahiko
AU - Mizuno, Tamaki
AU - Tahara, Tomomitsu
AU - Ohta, Yoshiji
AU - Nakano, Hiroshi
PY - 2006/4
Y1 - 2006/4
N2 - Background and Aims: Proton pump inhibitors (PPI) and prostaglandin (PG) preparations are believed to both prevent NSAID-induced gastric ulcers and promote the delayed healing of gastric ulcers by NSAIDs, but it remains unclear which of these drugs is superior. The aim of this study was to clarify which achieved better healing of NSAID-induced gastric ulcers, not only with respect to epithelialization but also repair of the submucosal tissues. Methods: We used acetic acid to induce gastric ulcers in rats, and compared the changes between a control group, NSAID group, NSAID+PPI group and NSAID + PG group. After removing the stomach of each animal, an ulcer index was calculated and the collagen content and type III collagen content of granulation tissue were measured. We also studied fibroblast dynamics, including proliferation, collagen synthesis, differentiation into myofibroblasts, and apoptosis. Results: lndomethacin prevented re-epithelialization of the ulcers, interfered with fibroblast function, and also delayed the replacement of type III collagen. Omeprazole promoted epithelialization, but could not fully reverse the influence of indomethacin on granulation tissue maturation. A concomitant dose with misoprostol reversed it completely. Conclusions: From our point of view in this study in the use of experimental ulcers, it was thought that compensation of PG should have priority to gastric acid inhibition in terms of healing of NSAID-induced gastric ulcer.
AB - Background and Aims: Proton pump inhibitors (PPI) and prostaglandin (PG) preparations are believed to both prevent NSAID-induced gastric ulcers and promote the delayed healing of gastric ulcers by NSAIDs, but it remains unclear which of these drugs is superior. The aim of this study was to clarify which achieved better healing of NSAID-induced gastric ulcers, not only with respect to epithelialization but also repair of the submucosal tissues. Methods: We used acetic acid to induce gastric ulcers in rats, and compared the changes between a control group, NSAID group, NSAID+PPI group and NSAID + PG group. After removing the stomach of each animal, an ulcer index was calculated and the collagen content and type III collagen content of granulation tissue were measured. We also studied fibroblast dynamics, including proliferation, collagen synthesis, differentiation into myofibroblasts, and apoptosis. Results: lndomethacin prevented re-epithelialization of the ulcers, interfered with fibroblast function, and also delayed the replacement of type III collagen. Omeprazole promoted epithelialization, but could not fully reverse the influence of indomethacin on granulation tissue maturation. A concomitant dose with misoprostol reversed it completely. Conclusions: From our point of view in this study in the use of experimental ulcers, it was thought that compensation of PG should have priority to gastric acid inhibition in terms of healing of NSAID-induced gastric ulcer.
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U2 - 10.1159/000092012
DO - 10.1159/000092012
M3 - Article
C2 - 16543735
AN - SCOPUS:33744479989
SN - 0012-2823
VL - 73
SP - 32
EP - 39
JO - Digestion
JF - Digestion
IS - 1
ER -