ABSTRACT
In the process of evolution a number of complicated mechanisms have developed to protect the gastric mucous membrane, e.g., angiogenesis and stimulation of mucosal growth. The aim of this study was to determine the role of vascular endothelial growth factor (VEGF) administered intraperitoneally in the gastroprotective response to stress-induced acute gastric ulcers in rats. A dramatic increase in the number of blood vessels was observed when VEGF was injected 24 h before stress exposure. Gastric secretion, depth of ulceration and ulceration index decreased significantly after VEGF application. The results demonstrate the gastroprotective effect of VEGF on stress-induced ulceration.
Subject(s)
Neovascularization, Physiologic/drug effects , Stomach Ulcer/prevention & control , Vascular Endothelial Growth Factor A/pharmacology , Animals , Disease Models, Animal , Gastric Mucosa/blood supply , Gastric Mucosa/drug effects , Injections, Intraperitoneal , Male , Rats , Rats, Wistar , Stomach Ulcer/physiopathology , Stress, Physiological , Stress, PsychologicalABSTRACT
Angiogenesis and VEGF play a major role in many repair processes such as healing of gastric ulceration. The present study was undertaken to assess the dynamics of changes in VEGF expression and angiogenesis in stress-induced gastric ulcers in rats. Acute gastric ulceration was induced using a water-immersion and restraint stress method. The VEGF expression, angiogenesis, size of area and depth of ulcers in gastric specimens were evaluated. The study shows that as early as one day after the development of ulcers there is a significant increase in both the expression of the VEGF protein and the number of newly formed microvessels, while an abrupt decrease in VEGF expression, observed on the fifth day, results in a decreased intensity of angiogenesis. Moreover, it has been demonstrated that the increase in VEGF expression and angiogenesis is accompanied by a reduction in the size of area and depth of stress-induced ulcers in rats. Six days after ulcer development both VEGF expression and angiogenesis return to normal levels.
