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Vol. 286, Issue 3, 1383-1390, September 1998
Department of Applied Pharmacology, Kyoto Pharmaceutical
University, Misasagi, Yamashina, Kyoto 607-8414, Japan
To elucidate the role of cyclooxygenase (COX)-2 in ulcer healing, we
compared the effects of NS-398 (COX-2-selective inhibitor) and
indomethacin (nonselective COX inhibitor) on the healing of acetic
acid-induced gastric ulcers in rats. Prostaglandin E2
(PGE2) production was elevated in ulcerated tissue, but
remained unaffected in intact tissue. COX-2 mRNA was only detected in
the ulcerated tissue, in which the COX-2 protein was found in
fibroblasts, macrophages/monocytes and granulocytes. In contrast, COX-1
mRNA expression was not affected by ulceration. In an in
vitro study, the increased PGE2 production was
inhibited by NS-398; this had no effect on PGE2 production in the intact tissue. When NS-398 and indomethacin were administered to
rats, 3 and 6 mg/kg NS-398 only reduced PGE2 production in the ulcerated tissue, but 10 mg/kg NS-398 and 0.5 to 2 mg/kg
indomethacin inhibited the production in both the ulcerated and intact
tissues. The healing of gastric ulcers was significantly impaired by 3 to 10 mg/kg NS-398 and 1 and 2 mg/kg indomethacin. The delay in ulcer
healing was associated with the inhibition of PGE2
production in the ulcerated tissue. As observed upon histological
analysis, regeneration of the mucosa, maturation of the ulcer base and
angiogenesis in the base were significantly prevented by 6 mg/kg NS-398
and 2 mg/kg indomethacin, although the inhibitory effect of NS-398 was
weaker than that of indomethacin. These results clearly indicate that
COX-2 plays an important role in the healing of gastric ulcers in rats.
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