Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2009 May 20:9:36.
doi: 10.1186/1471-230X-9-36.

Antiulcer activity of fluvoxamine in rats and its effect on oxidant and antioxidant parameters in stomach tissue

Hakan Dursun  1 , Mehmet Bilici, Fatih Albayrak, Cengiz Ozturk, Mustafa B Saglam, Hamit H Alp, Halis Suleyman
Affiliations

Antiulcer activity of fluvoxamine in rats and its effect on oxidant and antioxidant parameters in stomach tissue

Hakan Dursun et al. BMC Gastroenterol. .

Abstract

Background: Although many drugs are available for the treatment of gastric ulcers, often these drugs are ineffective. Many antidepressant drugs have been shown to have antiulcer activity in various models of experimental ulcer. One such drug, the antidepressant mirtazapine, has been reported to have an antiulcer effect that involves an increase in antioxidant, and a decrease in oxidant, parameters. To date, however, there is no information available regarding the antiulcer activity for a similar antidepressant, fluvoxamine. This study aimed to investigate the antiulcer effects of fluvoxamine and to determine its relationship with antioxidants.

Methods: Groups of rats fasted for 24 h received fluvoxamine (25, 50, 100 and 200 mg/kg), ranitidine (50 mg/kg) or distilled water by oral gavage. Indomethacin (25 mg/kg) was orally administered to the rats as an ulcerative agent. Six hours after ulcer induction, the stomachs of the rats were excised and an ulcer index determined. Separate groups of rats were treated with the same doses of fluvoxamine and ranitidine, but not with indomethacin, to test effects of these drugs alone on biochemical parameters. The stomachs were evaluated biochemically to determine oxidant and antioxidant parameters. We used one-way ANOVA and least significant difference (LSD) options for data analysis.

Results: The 25, 50, 100 and 200 mg/kg doses of fluvoxamine exerted antiulcer effects of 48.5, 67.5, 82.1 and 96.1%, respectively, compared to the control rat group. Ranitidine showed an 86.5% antiulcer effect. No differences were observed in the absence of indomethacin treatment for any dose of fluvoxamine or for ranitidine. The levels of antioxidant parameters, total glutathione and nitric oxide, were increased in all fluvoxamine groups and in the ranitidine group when compared with the indomethacin-only group. In addition, fluvoxamine and ranitidine decreased the levels of the oxidant parameters, myeloperoxidase and malondialdeyhyde, in the stomach tissues of the rats when compared to indomethacin group.

Conclusion: We conclude that fluvoxamine has antiulcer effects, and that these occur by a mechanism that involves activation of antioxidant parameters and inhibition of some toxic oxidant parameters.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Effects of fluvoxamine (FLU)+indomethacin (IND), ranitidine (RAN)+indomethacin (IND) and alone indomethacin (IND) on tGSH levels in the stomach tissues of rats. *Significant at p < 0.05 when compared to control.
Figure 2
Figure 2
Effects of fluvoxamine (FLU)+indomethacin (IND), ranitidine (RAN)+indomethacin (IND) and alone indomethacin (IND) on NO levels in the stomach tissues of rats. *Significant at p < 0.05 when compared to control.
Figure 3
Figure 3
Effects of fluvoxamine (FLU)+indomethacin (IND), ranitidine (RAN)+indomethacin (IND) and alone indomethacin (IND) on MPO levels in the stomach tissues of rats. *Significant at p < 0.05 when compared to control.
Figure 4
Figure 4
Effects of fluvoxamine (FLU)+indomethacin (IND), ranitidine (RAN)+indomethacin (IND) and alone indomethacin (IND) on MDA levels in the stomach tissues of rats. *Significant at p < 0.05 when compared to control.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Mózsik G, Jávor T. A biochemical and pharmacological approach to the genesis of ulcer disease. I. A model study of ethanol-induced injury to gastric mucosa in rats. Dig Dis Sci. 1988;33:92–105. doi: 10.1007/BF01536637. - DOI - PubMed
    1. Davies GR, Simmonds NJ, Stevens TR, Sheaff MT, Banatvala N, Laurenson IF, Blake DR, Rampton DS. Helicobacter pylori stimulates antral mucosal reactive oxygen metabolite production in vivo. Gut. 1994;35:179–185. doi: 10.1136/gut.35.2.179. - DOI - PMC - PubMed
    1. Ding SZ, Lam SK, Yuen ST, Wong BC, Hui WM, Ho J, Guo X, Cho CH. Prostaglandin, tumor necrosis factor alpha and neutrophils: causative relationship in indomethacin-induced stomach injuries. Eur J Pharmacol. 1998;348:257–163. doi: 10.1016/S0014-2999(98)00162-9. - DOI - PubMed
    1. Hooderwerf WA, Pasricha PJ. In: Goodman and Gilman's the pharmacological basis of therapeutics. Brunton L, editor. New-York: Mc Graw-Hill; 2006. Pharmacotherapy of gastric acidity, peptic ulcers, and gastroesophageal reflux disease; pp. 967–981.
    1. Brzozowski T, Konturek PC, Chlopicki S, Sliwowski Z, Pawlik M, Ptak Belowska A, Kwiecien S, Drozdowicz D, Pajdo R, Slonimska E, Konturek SJ, Pawli WW. Therapeutic potential of 1-methylnicotinamide against acute gastric lesions induced by stress: role of endogenous prostacyclin and sensory nerves. J Pharmacol Exp Ther. 2008;326:105–116. doi: 10.1124/jpet.108.136457. - DOI - PubMed

MeSH terms