The Effect of Portal Hypertension on the Glycoprotein Biosynthesis of Rat Gastric Mucosa

Abstract

The aim of this study was to assess the influence of epidermal growth factor (EGF) on glycoprotein biosynthesis in portal hypertensive (PHT) gastric mucosa. Portal-vein ligation (PVL) for a period of 4 weeks was applied to 40 male Wistar rats to produce experimental portal hypertension. The rats were subdivided into four groups. Human EGF was administrated to these four groups of animals at a does of 0, 10, 25, and 50 w g/kg/day for 7 days. An additional group of 10 rats without PVL and EGF pretreatment was employed as a control. The severity of gross gastric mucosal lesions was evaluated macroscopically by a gross ulcer index. Glycoprotein biosynthesis of the gastric mucosa was determined by the incorporation rate of [3 H]glucosamine. Quantitative changes of gastric mucosal hexosamines were also used for mucosal glycoproteins analyses. The gross mucosal damage was considerably greater in the PVL group without EGF pretreatment than in the EGF-pretreated groups (p < .05). The incorporation rate of [3 H]glucosamine was significantly higher in the control group and the EGF-pretreated groups than in the PVL group without EGF pretreatment (p < .05). Moreover, the incorporation rate of [3 H]glucosamine and the gastric mucosal hexosamine content were closely relevant to administration does of human EGF (p < .001). In addition, the reduction of glycoprotein biosynthesis was closely related to the increase in portal pressure (p = .001) and the severity of portal hypertensive gastropathy (p < .001). Our current study shows that the rate of incorporation of glucosamine is decreased in the PHT gastric mucosa and that EGF significantly stimulated glycoprotein synthesis in the PHT gastric mucosa. Accordingly, these findings may be helpful to explain the protective effect of EGF on the PHT gastric mucosa via increased glycoprotein biosynthesis in the stomach.