Effects Of High Salt Diet On TFF2 Expression In Gastric Mucosa Induced By H.pylori Infection In MGs

ObjectiveGastrointestinal diseases are the major diseases of the digestive system,and their occurrence is mainly related to infection factors(H.pylori)and environmental factors(high salt diet).Long-term chronic infection with H.pylori can lead to a variety of gastric diseases such as non-atrophic gastritis,atrophic gastritis,and gastric ulcers.At the same time,a long-term high-salt diet can also cause damage to the gastric mucosa.Trefoil factor 2(TFF2)is a small molecule polypeptide secreted by the gastrointestinal tract of mammals that can protect the gastric mucosa.The purpose of this study was to determine the effect of high-salt diet and H.pylori infection on the expression of TFF2 in gastric mucosa of Mongolian gerbils(MGs).MethodsIn this study,H.pylori,NCTC11637 strains,were selected for resuscitation and observation of the morphology of H.pylori in the culture medium.The culture results of H.pylori were identified by Gram staining.Eighty 6-week-old healthy male MGs were selected,and randomly divided into 4 groups including control group,H.pylori infection group,high-salt diet group,H.pylori+high-salt diet group,breeding 52 week,and established the MGs model induced by H.pylori infection.HE staining was used to diagnose the pathological changes of gastric mucosa of MGs.The infection of H.pylori in gastric mucosa was detected by Warthin-Starry staining,HE staining,and Giesma staining,The TFF2 expression levels of gastric mucosa were detected by immunohistochemical staining.Statistical software SPSS 19.0 was used for statistical analysis.H.pylori severity,pathological diagnosis results and expression of TFF2 in different groups were all analyzed by Fisher's exact test.The relationship between the degree of glandular injury and the expression of TFF2 was analyzed by Chi-square test.p<0.05 The difference was statistically significant.Results1.The H.pylori infection-induced MGs model was successfully established.In culture medium,H.pylori was translucent,scattered,needle-like colonies.By using Gram staining,H.pylori showed red,curved,rod-shaped colonies.In gastric mucosa,the results of HE staining,Warthin-Starry silver staining,and Giemsa staining showed that H.pylori is located in the mucous layer,gastric pit,or glandular cavity on the surface of the gastric mucosa,and "S"-shaped curved or rod-shaped bacteria.2.The severity of H.pylori in the H.pylori+high salt diet group was significantly higher than that in the H.pylori infection group.H.pylori identification in stomach tissue showed that H.pylori infection rate reached 100%in H.pylori infection group and H.pylori+high salt diet group.The infection degree of H.pylori ranged from + to++.H.pylori infection intensity in the H.pylori+high-salt diet group(62.50%,10/16)was significantly higher than that in the H.pylori infection group(16.67%,3/18).3.The severity of H.pylori was positively correlated with the severity of gastric disease.All MGs of H.pylori infected group and H.pylori+high-salt diet groups were divided into H.pylori(+)group and H.pylori(++)group.In the H.pylori(++)group,the incidence of parietal cell necrosis was 62%(8/13),and significantly higher than that in the H.pylori(+)group(24%,5/21);the incidence of interstitial fibrosis was 62%(8/13),and significantly higher than 5%(1/21)of the H.pylori(+)group;the incidence of glandular atrophy was 23%(3/13),and significantly higher than that of the H.pylori(+)group.Therefore,the heavier the H.pylori infection,the heavier the severity of gastric disease.4.The severity of gastric disease in the H.pylori+high salt diet group was higher than that in the H.pylori infection group.Histopathological examination revealed that necrosis of parietal cells occurred in 63%(10/16)in the H.pylori + high salt diet group,which was significantly higher than that in the H.pylori infection group(22%,4/18);The percentage of interstitial fibrosis in the gastric mucosa of the MGs with 38%(6/16)was significantly higher than that in the H.pylori infection group(6%,1/18).Therefore,the severity of gastric disease in the H.pylori+high salt diet group was significantly higher than that in the H.pylori infection group.5.In H.pylori infection group,61%(11/18)were high expression of TFF2,which was significantly higher than that in control group 15%(3/20);In H.pylori + high salt diet group,25%(4/16)animals were high expression of TFF2,and significantly lower than the H.pylori infection group.6.The expression level of TFF2 depends on the degree of damage of glands.The more severe the damage of glandular cells,the lower the expression level of TFF2.According to whether the glandular cells were reduced,all the MGs in the four groups were divided into normal gastric mucosa(24),non-adenocytopenia lesions(29),and glandular cell degeneration(20).Among the MGs with reduced cytopathogenicity,15%(3/20)of MGs had high expression of TFF2 in gastric mucosa,which was significantly lower than that of non-adenocytopenia(48%,14/29).Therefore,the more severe the damage of glandular cells,the lower the expression level of TFF2.Conclusions1.H.pylori can colonize the gastric mucosa of MGs and persist for a long time,leading to the occurrence of different gastric diseases.2.High-salt diets are more prone to H.pylori infection,which exacerbates gastric mucosal damage caused by H.pylori infection.3.H.pylori infection can upregulate the expression of TFF2 in gastric mucosa of MGs,but high-salt diet will reduce the number of glandular cells by increasing the degree of H.pylori-indnced gastric mucosal injury,and thus down-regulate the expression of TFF2 in H.pylori-infected MGs gastric mucosa.