Abstract
to evaluate the influence of Duodenal reflux in histological changes of the gastric mucosa of rats infected with Helicobacter pylori submitted to pyloroplasty. after two weeks of acclimation, we infected 30 male Wistar rats with Helicobacter pylori. We randomly divided them into three groups: one submitted to pyloroplasty, another to partial gastrectomy and the third, only infected, was not operated. After six months of surgery, euthanasia was carried out. Gastric fragments were studied by light microscopy to count the number of H. pylori, and to observe the histological changes (gastritis, metaplasia, dysplasia and neoplasia). We confirmed these changes by immunohistochemistry using the molecular markers PCNA and TGF-beta. the animals submitted to pyloroplasty had higher percentage of colonization by H. pylori (median=58.5; gastrectomy=16.5; control=14.5). There was a positive correlation between the amount of H. pylori and the occurrence of chronic gastritis present in the antral fragments. Neoplasia occurred in 40% of rats from the group submitted to pyloroplasty. The staining with PCNA and TGF-ß confirmed the histopathological changes visualized by optical microscopy. the antral region was the one with the highest concentration of H. pylori, regardless of the group. There was a positive correlation between the appearance of benign disorders (chronic gastritis, metaplasia, dysplasia) and cancer in mice infected with H. pylori submitted to pyloroplasty. avaliar a influência do refluxo duodenogástrico nas alterações histológicas da mucosa gástrica de ratos, infectados por Helicobacter pylori, submetidos à piloroplastia. após duas semanas de aclimatação, 30 ratos machos da raça Wistar, foram infectados com o microorganismo patogênico H. pylori. De forma aleatória, foram divididos em três grupos: um submetido à piloroplastia, outro à gastrectomia parcial e o terceiro, apenas infectados, não foi operado. Após seis meses de operados, procedeu-se a eutanásia. Os fragmentos gástricos foram estudados por microscopia óptica, para a contagem da quantidade de H. pylori, e para a observação das alterações histológicas (gastrite, metaplasia, displasia e neoplasia). A confirmação dessas alterações foi feita por imuno-histoquímica, utilizando os marcadores moleculares PCNA e TGFbeta. os animais submetidos à piloroplastia tiveram maior percentual de colonização por H. pylori (mediana=58,5; gastrectomia=16,5; controle=14,5). Houve correlação positiva entre quantidade de H. pylori e ocorrência de gastrite crônica presente nos fragmentos do antro. Ocorreu 40% de neoplasia no grupo submetido à piloroplastia. A marcação de PCNA e TGF-beta confirmou as alterações histopatológicas visibilizadas à microscopia óptica. a região do antro foi a que apresentou a maior concentração de H. pylori, independente do grupo. Houve correlação positiva entre e o aparecimento de alterações benignas (gastrite crônica, metaplasia, displasia), e de neoplasia nos ratos infectados com H. pylori submetidos à piloroplastia.
Highlights
Gastric cancer, a public health problem worldwide, continues to be the most common malignancy of the digestive tract in humans, especially among the elderly[1,2]
Several factors are involved in the genesis of gastric cancer, such as environmental and dietary factors, with emphasis on foods rich in nitrates and nitrites, H. pylori infection and duodenogastric reflux[6,7,8]
We considered the study of the gastric mucosa: (a) Normal- absence of neutrophils and the presence of up to ten lymphocytes and plasma cells in the lamina propria per 400X microscopic field; (b) Chronic gastritispresence of predominantly mononuclear cells; we measured chronicity by the density of the lymphocyte, plasma cells and polymorphonuclear cells infiltration in the lamina propria Gastritis and its activity followed the modified Sydney classification[14]; (c) Metaplasia- presence of intestinal cells in the stomach mucosa; (d) Dysplasia- distortion of intraepithelial cytoarchitecture; (e) Neoplasia- same features of dysplasia plus extraepithelial invasion
Summary
A public health problem worldwide, continues to be the most common malignancy of the digestive tract in humans, especially among the elderly[1,2]. But its prognosis little changed in recent years due to diagnosis made at an advanced stage of disease progression[3,4,5]. Several factors are involved in the genesis of gastric cancer, such as environmental and dietary factors, with emphasis on foods rich in nitrates and nitrites, H. pylori infection (a gram-negative spiral bacterium that is often associated with chronic gastritis, intestinal metaplasia and dysplasia) and duodenogastric reflux[6,7,8]. Depending on the rhythm, volume and duration of gastric mucosal exposure, it can be highly pathogenic, by changing the physicochemical characteristics of the protective mucus layer, increase gastric pH, favoring bacterial and n-compounds proliferation[10,11,12]
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