Inhibition of inducible nitric oxide synthase delays gastric ulcer healing in the rat

Yasutada Akiba, Masahiko Nakamura, Mikiji Mori, Hidekazu Suzuki, Masaya Oda, Hiroyuki Kimura, Soichiro Miura, Masaharu Tsuchiya, Hiromasa Ishii

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43 Citations (Scopus)


We sought to clarify the role of nitric oxide (NO) generated from inducible NO synthase (iNOS) during healing of rat gastric ulcers. After gastric ulcers were induced by acetic acid, rats were treated with vehicle, N(G)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG), and dexamethasone (Dex) by gastric intubation twice a day for 3 days to 1 week. L-NAME significantly delayed healing compared with vehicle. AG and Dex significantly reduced ulcer size 3 days after ulcer induction but did not further reduce ulcer size 1 week after induction. iNOS expression was present in inflammatory cells, some epithelial cells, and in vascular smooth muscle in the regenerating mucosa of the vehicle-treated group. However, the number of iNOS-positive inflammatory cells increased in the AG- and L-NAME-treated groups. AG and L-NAME significantly increased the number of inflammatory cells with endogenous peroxidase and significantly reduced the number of apoptotic inflammatory cells compared with vehicle. In conclusion, inhibition of iNOS increases the number of inflammatory cells in the ulcer margin and delays ulcer healing. These observations suggest that NO generated from iNOS not only participates in ulcer formation but also plays a beneficial role in ulcer healing, in part by the exclusion of iNOS-positive inflammatory cells from the regenerating mucosa.

Original languageEnglish
Pages (from-to)S64-S73
JournalJournal of Clinical Gastroenterology
Issue numberSUPPL. 1
Publication statusPublished - 1998 Dec 1


  • Apoptosis
  • Inducible nitric oxide synthase
  • Inflammatory cells
  • Nitric oxide
  • Ulcer healing

ASJC Scopus subject areas

  • Gastroenterology


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