THE LEVEL OF REDOX-RESPONSIVE TRANSCRIPTION FACTOR EGR-1, SP-1 AND HIF-1 UNDER CONDITIONS OF ETHANOL-INDUCED GASTRIC LESIONS

Changes in redox status of gastric mucosa cells are the main pathogenic factor of gastric erosion and gastric ulcer development. Egr-1, Sp-1 and Hif-1α – are the hypoxia-sensitive transcription factors that respond to hypoxic changes in cells and are involved in the pathogenesis of gastric ulcer. The role of hypoxia-sensitive transcription factors during ethanol-induced gastric lesions studied not enough, so the aim of this study was to test the involvement Egr-1, Sp-1 and Hif-1α in the pathogenesis of ethanol-induced gastric lesions. The investigations were conducted on white male rats with weight of 180-220 g. For modeling of ethanol-induced gastric lesions, experimental groups of rats were injected intragastricaly 1 ml of 96% ethanol. Control groups of rats were administered 1 ml of saline. In the gastric mucosa of rats was determined protein expression by Western blot analysis. 20 minutes of ethanol exposure caused the massive hemorrhages and erosions. Increased exposure time was associated with worsened clinical picture. We have established decrease in the content of hypoxia-sensitive transcription factor Hif-α after 1 hour ethanol exposure, that was associated with pathological changes in gastric mucosa of rats. The content of transcription factor Egr-1 remained unchanged during the entire experiment. Since Sp-1 competes for binding sites with Egr-1, we tested the hypothesis that Sp-1 - main transcription factor for this pathology. We found that 20 minutes and 1 hour of ethanol exposure induced increasing of Sp-1 content. The results of expression of hypoxia-sensitive transcription factors in rats gastric mucosa in response to ethanol requires further studying. We concluded that under the conditions of ethanol-induced gastric ulcers there are multidirectional changes in the level of redox-sensitive transcription factors, including Egr -1, Sp -1 and Hif - 1. Sp-1 - plays a key role in the pathogenesis of this disease.