RESUMO
To elucidate the mechanisms of antiulcerogenic agents, we established the cell culture model derived from rat gastric epithelium. The cultured cells were identified as mucus-producing cells by using histological analysis. This culture model is useful for investigating the untiulcer effect of various agents and to reveal the mechanisms of the drug action. In particular, the ulcer-healing model using the cultured monolayer is promising and convenient for the study of several growth factors such as HGF as well as antiulcerogenic agents. The effect of polaporezinc in the cultured model is introduced.
Assuntos
Antiulcerosos/farmacologia , Carnosina/análogos & derivados , Carnosina/farmacologia , Mucosa Gástrica/efeitos dos fármacos , Compostos Organometálicos/farmacologia , Animais , Divisão Celular/efeitos dos fármacos , Células Cultivadas , Grupo dos Citocromos c/metabolismo , DNA/biossíntese , Feminino , Mucosa Gástrica/citologia , Mucosa Gástrica/ultraestrutura , Fator de Crescimento de Hepatócito/farmacologia , Peróxido de Hidrogênio/toxicidade , Masculino , Microscopia Eletrônica , Ratos , Compostos de ZincoRESUMO
Migration of epithelial cells (restitution) is an essential step in the repair of gastric mucosal lesions. Although a variety of growth factors are reported to facilitate gastric epithelial restitution, the intracellular mechanisms of this process are not fully understood. In this study we investigated the effects of hepatocyte growth factor (HGF) on restitution of normal rat gastric epithelial RGM-1 cell monolayers after injury and examined whether cyclooxygenase-2 (COX-2) is involved in HGF-mediated epithelial restitution. Restitution of RGM-1 monolayers was assessed using a round wound restitution model. Application of HGF (5 ng/ml) significantly facilitated the restitution of RGM-1 monolayers after artificial wounding. HGF also induced expression of COX-2 protein in RGM-1 cells, and wounding itself induced COX-2 expression in the cells located at the edge of the wound. Inhibition of COX-2 activity by NS-398, a specific COX-2 inhibitor, significantly delayed the HGF-mediated restitution. These results suggest the involvement of COX-2 in the action of HGF on gastric epithelial restitution.