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World J Gastroenterol. May 14, 2012; 18(18): 2147-2160
Published online May 14, 2012. doi: 10.3748/wjg.v18.i18.2147
Published online May 14, 2012. doi: 10.3748/wjg.v18.i18.2147
Figure 6 Effects of various prostaglandin E agonists on gastric lesions generated by indomethacin in rats.
The animals were given indomethacin (30 mg/kg) s.c. and killed 4 h later. Prostaglandin E2 (PGE2, 0.3 mg/kg), 17-phenyl PGE2 (0.3 mg/kg; EP1 agonist), sulprostone (0.3 mg/kg; EP1/EP3 agonist), butaprost (10 mg/kg; EP2 agonist), ONO-NT-012 (10 mg/kg; EP3 agonist) and 11-deoxy PGE1 (3 mg/kg; EP3/EP4 agonist) were given i.v. 10 min before indomethacin. Data are presented as the mean ± SE in 4-6 rats. aP < 0.05 vs control (data from ref. 39 after modification).
- Citation: Takeuchi K. Pathogenesis of NSAID-induced gastric damage: Importance of cyclooxygenase inhibition and gastric hypermotility. World J Gastroenterol 2012; 18(18): 2147-2160
- URL: https://www.wjgnet.com/1007-9327/full/v18/i18/2147.htm
- DOI: https://dx.doi.org/10.3748/wjg.v18.i18.2147