Transretinoic acid inhibits rats gastric epithelial dysplasia induced by N-methyl-N-nitro-N-nitrosoguanidine: influences on cell apoptosis and expression of its regulatory genes

Gastric epithelial dysplasia (GED) hypothetically is a straight-forward concept: dysplastic epithelium replacing the normal gastric epithelium of the stomach[1]. In the stomach, like any other segment of the gut, it is defined as an unequivocal non-invasive epithelial change[2,3]. The observation of gastric dysplasia as a cancerous lesion was recognized over a century ago, but it is only after the advent of gastroscopy that its clinical significance has been stressed[4-7]. All-trans retinoic acid can effectively reverse dysplasia in gastric epithelial cells, thereby inhibiting its progression to gastric cancer[8-10]. However, its mechanism is not yet clear. We used N-methyl-N-nitro-N-nitrosoguanidine (MNNG) to establish a rat model of gastric epithelial cell dysplasia, and to study the influence of all-trans retinoic acid. Changes in apoptosis and expression of Bcl-2, Fas and ICE were observed to investigate into insight of its mechanism.