Histological Change and Expression of p16, Bcl-2 and Proliferating Cell Nuclear Antigen in Atrophic Gastric Mucosa in Rats

Background:Chronic atrophic gastritis, especially antral atrophic gastritis, is closely related with gastric cancer. Dysregulation of cell proliferation and apoptosis plays an important role in the malignant change of gastric mucosa. Aims:To investigate the histological change and expression of p16, Bcl-2 and proliferating cell nuclear antigen (PCNA) in atrophic gastric mucosa in rats so as to appraise the effect of these regulators on the formation of atrophic gastritis. Methods:Chronic atrophic gastritis was induced by ammonia, sodium deoxycholate and alcohol administration. The rats were divided into normal control group and model group, and were sacrificed 2, 4 and 6 months later, respectively. Gastric mucosa was taken for the observation of morphological and histological changes. Expression of p16, Bcl-2 and PCNA in antral mucosa were determined by immunohistochemical method. Results:Gastric antral mucosa of the model rats showed obvious inflammatory cell infiltration with gastric pit hyperplasia, the thickness and number of glands decreased significantly;changes of gastric body mucosa were mild, only with the number of parietal cells reduced at the 6th month. During the process of antral mucosal atrophy, the expression of p16 decreased and that of Bcl-2 and PCNA increased gradually. Expression of p16 was lower and expression of Bcl-2 and PCNA was higher in atrophic group than those in non-atrophic group. Conclusions:Multifactorial long term chronic stimulation may lead to gastric mucosa atrophy in rats. Gastric mucosa of model rat is in a hyper-proliferation status, with low protein expression of anti-oncogene p16 and high protein expression of apoptosis suppressor gene Bcl-2. Development of atrophic gastritis has some correlation with the imbalance between cell proliferation and apoptosis.