UNLABELLED: We evaluated whether monolayers from a well-differentiated human gastric epithelial cell line (MKN 28) are suitable for studying the effect of drugs on gastric mucosa. MKN 28 monolayers and monolayers of human gastric epithelial cells from surgical specimens were studied morphologically and functionally. The protective effect of acetaminophen against taurocholate-induced damage was evaluated as was its effect on prostaglandin production. Both types of cultures showed similar morphologic and histochemical characteristics. Indomethacin inhibited and arachidonic acid stimulated prostaglandin production by both types of monolayers similarly. Both monolayers responded similarly to drug-induced damage. Acetaminophen decreased taurocholate-induced damage by 33% and 40% in MKN 28 cells and in primary human gastric cell culture, respectively. Indomethacin did not prevent acetaminophen protection nor did the amount of prostaglandin produced by cells increase after incubation with acetaminophen. IN CONCLUSION: (1) in the MKN 28 cell line model acetaminophen protected against taurocholate-induced damage; the percentage of protection was similar to that in primary cultures of human gastric epithelial cells; (2) acetaminophen protection in both models was not related to increased prostaglandin production; (3) the MKN 28 cell line is a suitable model to study damage to and protection of gastric epithelial cells in vitro.
UNLABELLED: We evaluated whether monolayers from a well-differentiated human gastric epithelial cell line (MKN 28) are suitable for studying the effect of drugs on gastric mucosa. MKN 28 monolayers and monolayers of human gastric epithelial cells from surgical specimens were studied morphologically and functionally. The protective effect of acetaminophen against taurocholate-induced damage was evaluated as was its effect on prostaglandin production. Both types of cultures showed similar morphologic and histochemical characteristics. Indomethacin inhibited and arachidonic acid stimulated prostaglandin production by both types of monolayers similarly. Both monolayers responded similarly to drug-induced damage. Acetaminophen decreased taurocholate-induced damage by 33% and 40% in MKN 28 cells and in primary human gastric cell culture, respectively. Indomethacin did not prevent acetaminophen protection nor did the amount of prostaglandin produced by cells increase after incubation with acetaminophen. IN CONCLUSION: (1) in the MKN 28 cell line model acetaminophen protected against taurocholate-induced damage; the percentage of protection was similar to that in primary cultures of human gastric epithelial cells; (2) acetaminophen protection in both models was not related to increased prostaglandin production; (3) the MKN 28 cell line is a suitable model to study damage to and protection of gastric epithelial cells in vitro.
Authors: J Suzuki; H Ohnsihi; H Shibata; A Wada; T Hirayama; T Iiri; N Ueda; C Kanamaru; T Tsuchida; H Mashima; H Yasuda; T Fujita Journal: J Clin Invest Date: 2001-02 Impact factor: 14.808
Authors: V Ricci; C Ciacci; R Zarrilli; P Sommi; M K Tummuru; C Del Vecchio Blanco; C B Bruni; T L Cover; M J Blaser; M Romano Journal: Infect Immun Date: 1996-07 Impact factor: 3.441
Authors: N Okayama; M R Fowler; S R Jennings; R Specian; B Alexander; T H Jackson; T Oshima; T Shannon; J S Alexander Journal: In Vitro Cell Dev Biol Anim Date: 2000-04 Impact factor: 2.416