| Background and purposeHelicobacter pylori(H.pylori)infection and Chronic atrophic gastritis(CAG)[1-2],closely related diseases such as gastric cancer[3],the Hp infections worldwide high proportion,although only a small number of people have the possibility of development for the disease,but the direction is unpredictable,therefore,has brought the global health system must burden.The presence of helicobacter pylori cagA contributes to the colonization of gastric epithelium and the release of inflammatory factors.The presence of the vacA contributes to the persistence of colonization and aggravation of the inflammatory response.Sustained infection of H.pylori can lead to chronic persistent inflammation and dysregulation of cell signal transduction,which can induce the production of chemokines,cytokines,free radicals,matrix metalloproteinases,etc.This process further increases the risk of disease development into CAG and gastric cancer.In addition,according to the investigation,most of the people's diet contains excessive salt,but the high-salt diet will cause damage to the gastric epithelium,leading to the proliferation of gastric pits and the reduction of parietal cells,which increases the risk of CAG disease.Among them,the disease with imbalance between proliferation and apoptosis develops into gastric cancer,and the high-salt diet can promote the colonization of Hp.CAG is a precancerous disease of gastric cancer.However,both of them are highly correlated with H.pylori and high-salt diet.In order to prevent CAG from developing into gastric cancer and reduce the incidence and mortality of gastric cancer,timely diagnosis and treatment of CAG is extremely important.Most studies of H.pylori infection in mice use female mice.That standard inbred mouse strains(including C57BL/6 and BALB/c)have been involved,while inbred C57BL/6 mice are more prone to H.pylori colonization than other strains.Male mice are significantly more prone to H.pylori colonization than female[4].Hp was colonized in C57BL/6 mice[5].This experiment will use inbred line,male C57BL/6 mice,Hp SS1 strains of H.pylori,and high-salt diet were to establish the H.pylori and high-salt related CAG model,and use this model to investigate gastric secrete element-17(Gastrin-17,G-17)for screening the CAG application value,comparative model of inflammatory factor levels of interleukin 8(IL-8),and provide related to the CAG treatment of the late model,to help prevent the CAG for the development of gastric cancer.Materials and methods40 male C57BL/6 mice of SPF level,weight 22-24g and age 5-7 weeks were randomly divided into group A(blank control group),group B(high salt group),group C(H.pylori group)and group D(high salt+H.pylori group),with 10 mice in each group.Group A:ultrapure water was administered to the mice,each of which was 0.3ml·times-1·days-1.Group B:each mouse was given 1.8%Nacl solution by intragastric administration,0.3ml·times-1·days-1.Group C:mice were given 1×109CFU/mL H.pylori bacterial suspension by gavage,each of which was 0.3ml·times-1,once every 1 day,for a total of 6 times.Group D:mice were administered with 1.8%Nacl solution+1×109CFU/mL H.pylori bacterial suspension in the same manner as groups B and C.In the experiment,the feed was removed 12 hours before gavage,followed by feeding and free drinking during the experiment.At the end of week 16 and the end of week 24,5 mice in each group were sacrificed to observe the changes in body weight of each group,the colonization of Hp was observed by immunohistochemistry,the histopathological changes of gastric mucosa were observed by HE staining,and the expression levels of serum g-17 and il-8 were detected by enzyme linked immunosorbent assay(ELISA).Results1.Urease test:at the end of the 16th week,groups A and B showed negative results,while groups C and D showed positive results.At weekend 24,the results of Hp colonization in gastric mucosa of mice in each group were the same as at weekend 16.Immunohistochemistry:no H.pylori colonization was observed in the gastric mucosa of group A and group B at the end of the 16th week,while H.pylori colonization was observed in the gastric mucosa of mice in groups C and D.2.Weight changes of mice:At 2-18 weeks,the body weight of mice in group B,C and D was not significantly lower than that in group A(P>0.05).At the 20th week,compared with group A,the body weight of group B and group C decreased,but there was no significant difference(P>0.05).Compared with group A,the body weight of group D decreased significantly(P<0.05).At 22-24 weeks,the body weight of group B,C and D all decreased significantly compared with group A(P<0.05).3.Gastric pathology and histological changes in mice:Visual observation:at week 16,the gastric mucosa of mice in group A was orange and the folds were regular.Compared with group A,the gastric mucosa of group C was lighter and the folds were irregular.The color of gastric mucosa in group B and D became pale,and the folds became irregular and shallow.At week 24,the gastric mucosa of group A was not significantly different from that of group A at week 16.In group B,C and D,the color of gastric mucosa was white,and the gastric folds were irregular and low.HE:At week 16,the gastric mucosa epithelium in group A was completely continuous,and the glands were arranged in A dense and regular manner.No glands became thinner and narrower in thickness,and inflammatory cell infiltration was occasionally observed in the lamina propria.The gastric mucosa epithelium in group B was discontinuous,the mucosa became thinner,and the glandular distribution became sparse and slightly reduced,with little inflammatory cell infiltration visible.The epithelial cells on the gastric mucosal surface of group C were damaged,and the distribution and number of glands were not significantly abnormal,indicating inflammatory cell infiltration.In group D,the gastric mucosa was thinner,the glands were thinner and slightly reduced,the arrangement was disorderly,the glandular ducts were enlarged,and inflammatory cell infiltration was observed in the lamina propria.At week 24,there was no significant change in gastric mucosa between week 16 and group A.The gastric mucosa cells in group B were damaged and thinned,and the glandular distribution was sparse and moderately reduced.The number of infiltrated inflammatory cells was slightly increased compared with that at week 16.The surface of gastric mucosal epithelial cells in group C was discontinuous and the mucosa became thinner,the gland distribution was sparse and slightly reduced,and the amount of inflammatory cell infiltration was increased.In group D,the epithelial cells on the mucosal surface were destroyed,the mucosa became thinner,the glands were sparse and moderately reduced,the glandular ducts were enlarged,and the number of inflammatory cells infiltrated increased.Mucosa and lamina propria thickness:at week 16,compared with group A and C,the gastric mucosa and lamina propria thickness of mice in groups B and D became thinner and showed significant difference(P<0.05).At week 24,compared with group A,the thickness of gastric mucosa and lamina propria in group B,C and D significantly decreased(P<0.05).Inflammation score:at week 16 and 24,there was no significant difference in chronic inflammation score between groups A,B,C and D(P>0.05).Compared with groups A and B,the score of active inflammation in groups C and D increased,and the difference was significant(P<0.05).4.Changes of serum g-17 level in mice:At week 16,compared with group A,g-17 in groups B,C and D was not significantly increased(P>0.05).At week 24,serum g-17 levels in groups B and D were lower than those in group A(P<0.05).5.Changes of serum il-8 level in mice:At week 16 and 24,higher levels of serum il-8 were found in groups C and D than in groups A and B(P<0.05).Conclusion1.High salt can accelerate the establishment of CAG model.2.Preliminary screening of CAG by g-17 has certain application value.3.H.pylori can affect the change of gastric inflammation level,while high-salt diet does not significantly affect the change of inflammation. |
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