Duodenogastric Reflux Increases the Penetration of N-3H-Methyl-N-nitro-N-nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis

Background: The updated model for the mechanism of gastric carcinogenesis demonstrates that Helicobacter pylori (H. pylori) is a risk factor in every step of the process. The expression of certain gastric mucins is altered by H. pylori infection in adult patients. The aim of our research was to assess the impact of H. pylori infection on the expression of secretory mucins in the pediatric antral mucosa. Methods: Slides were stained with monoclonal antibodies for MUC5AC, MUC6 and MUC2, digitalized and scored using both a semiquantitative and a quantitative approach. Results: The expression of MUC5AC was significantly lower in infected children. Also, MUC2 expression was more pronounced in infected children. MUC6 expression did not differentiate between infected and noninfected children. Additionally, the presence of chronic inflammation significantly altered the expression of MUC6 and MUC2. The expression of MUC6 was significantly higher in patients with gastric atrophy. Conclusion: The minor differences in mucin expression at distinct ages might stem from different H. pylori exposure periods. Further research is needed to determine the particular patterns of expression according to age and to evaluate the effects of the interaction between H. pylori and mucins in the progression of the gastric carcinogenesis cascade.

Download Full-text

The Role of PPARγinHelicobacter pyloriInfection and Gastric Carcinogenesis

PPAR Research ◽

10.1155/2012/687570 ◽

2012 ◽

Vol 2012 ◽

pp. 1-6 ◽

Cited By ~ 5

Author(s):

Jong-Min Lee ◽

Sung Soo Kim ◽

Young-Seok Cho

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Current Knowledge ◽

Mucosal Injury ◽

Gastric Carcinogenesis ◽

Etiologic Factor ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

H Pylori

Peroxisome proliferator-activated receptorγ(PPARγ) is a nuclear receptor that is important in many physiological and pathological processes, such as lipid metabolism, insulin sensitivity, inflammation, cell proliferation, and carcinogenesis. Several studies have shown that PPARγplays an important role in gastric mucosal injury due toHelicobacter pylori(H. pylori). AsH. pyloriinfection is the main etiologic factor in chronic gastritis and gastric cancer, understanding of the potential roles of PPARγinH. pyloriinfection may lead to the development of a therapeutic target. In this paper, the authors discuss the current knowledge on the role of PPARγinH. pyloriinfection and its related gastric carcinogenesis.

Download Full-text

Eugenol inhibits cell proliferation via NF-κB suppression in a rat model of gastric carcinogenesis induced by MNNG

Investigational New Drugs ◽

10.1007/s10637-009-9345-2 ◽

2009 ◽

Vol 29 (1) ◽

pp. 110-117 ◽

Cited By ~ 45

Author(s):

P. Manikandan ◽

G. Vinothini ◽

R. Vidya Priyadarsini ◽

D. Prathiba ◽

S. Nagini

Keyword(s):

Cell Proliferation ◽

Rat Model ◽

Gastric Carcinogenesis

Download Full-text

M1634 Overexpression of Retinoic Acid-Regulated Nuclear Matrix-Associated Protein (RAMP) Induces Cell Proliferation in Gastric Cancer: Potential Oncogenic Role of Ramp in Gastric Carcinogenesis

Gastroenterology ◽

10.1016/s0016-5085(08)61804-1 ◽

2008 ◽

Vol 134 (4) ◽

pp. A-386

Author(s):

Julia J. Li ◽

Enders K. Ng ◽

Yu P. Ng ◽

Jun Yu ◽

Joseph J. Sung ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Retinoic Acid ◽

Nuclear Matrix ◽

Gastric Carcinogenesis

Download Full-text

Effects of the duodenogastric reflux on cell proliferation and carcinogen penetration in the gastric mucosa of rats

Gastroenterology ◽

10.1016/s0016-5085(00)83207-2 ◽

2000 ◽

Vol 118 (4) ◽

pp. A281

Author(s):

Kjell K. Ovrebo ◽

Knut Svanes ◽

Steinar Kvinnsland ◽

Ketil Grong ◽

Hafdan Sorbye

Keyword(s):

Cell Proliferation ◽

Gastric Mucosa ◽

Duodenogastric Reflux

Download Full-text

Gastric carcinogenesis in the rat induced by duodenogastric reflux without carcinogens: morphology, mucin histochemistry, polyamine metabolism, and labelling index.

Gut ◽

10.1136/gut.32.12.1447 ◽

1991 ◽

Vol 32 (12) ◽

pp. 1447-1454 ◽

Cited By ~ 39

Author(s):

P R Taylor ◽

R C Mason ◽

M I Filipe ◽

S Vaja ◽

D C Hanley ◽

...

Keyword(s):

Duodenogastric Reflux ◽

Gastric Carcinogenesis ◽

Labelling Index ◽

Polyamine Metabolism ◽

Mucin Histochemistry

Download Full-text

Does troncular vagotomy modify the proliferative gastric lesions induced in rats by duodenogastric reflux?

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502007000300009 ◽

2007 ◽

Vol 22 (3) ◽

pp. 210-214 ◽

Cited By ~ 5

Author(s):

Paulo Antônio Rodrigues ◽

Shoiti Kobayasi ◽

Maria Aparecida Marchesan Rodrigues

Keyword(s):

Gastric Mucosa ◽

Gastric Wall ◽

Duodenogastric Reflux ◽

Biological Behavior ◽

Jejunal Loop ◽

Antral Mucosa ◽

Benign Lesions ◽

Pyloric Mucosa ◽

Male Wistar Rats ◽

Anterior Gastric Wall

PURPOSE: to investigate if combining VT to DGR through the pylorus can modulate the biological behavior of PL induced by DGR and to verify if TV alone can induce morphologic lesions in the gastric mucosa. METHODS: 62 male Wistar rats were assigned to four groups: 1 - Control (CT) gastrotomy; 2 - Troncular Vagotomy (TV) plus gastrotomy; 3 - Duodenogastric reflux through the pylorus (R) and 4 - Troncular vagotomy plus DGR (RTV). The animals were killed at the 54 week of the experiment. DGR was obtained by anastomosing a proximal jejunal loop to the anterior gastric wall. TV was performed through isolation and division of the vagal trunks. Gastrotomy consisted of 1 cm incision at the anterior gastric wall. PL were analyzed gross and histologically in the antral mucosa, at the gastrojejunal stoma and at the squamous portion of the gastric mucosa. RESULTS: Groups R and RTV developed exophytic lesions in the antral mucosa (R=90.9%; RTV=100%) and at the gastrojejunal stoma (R=54.54%; RTV=63.63%). Histologically they consisted of proliferative benign lesions, without cellular atypias, diagnosed as adenomatous hyperplasia. Both groups exposed to DGR presented squamous hyperplasia at the squamous portion of the gastric mucosa (R= 54.5%; RTV= 45.4%). TV, alone, did not induce gross or histological alterations in the gastric mucosa. TV did note change the morphologic pattern of the proliferative lesions induced by DGR. CONCLUSIONS: DGR induces the development of PL in the pyloric mucosa and at the gastrojejunal stoma. TV does not change the morphologic pattern of the proliferative lesions induced by DGR. TV alone is not able to induce morphologic lesions in the gastric mucosa.

Download Full-text