脾虚蒙古沙土鼠感染幽门螺杆菌动物模型的建立

目的 :建立脾虚蒙古沙土鼠感染幽门螺杆菌 (Hp)动物模型 ,验证该模型出现的病理改变及 Hp定植情况。方法 :采用国际标准菌株 SS1灌喂利血平致脾虚蒙古沙土鼠 ,建立脾虚蒙古沙土鼠感染 Hp动物模型 (8只 ) ,检测胃粘膜 Hp定植量、炎症程度 ,并与脾虚组、Hp感染组及正常组 (各 8只 )对照。结果 :脾虚 Hp感染组大鼠胃粘膜 Hp定植量显著增加 ,炎症程度随之加重 (P <0 .0 1) ;脾虚组胃粘膜炎症程度差异无显著性意义 (P >0 .0 5 )。结论 :脾胃虚弱可能是 Hp感染的病理基础 ,脾虚感染 Hp蒙古沙土鼠动物模型的建立对研究 Hp感染的中医致病机制 ,评价中药治疗 Hp的疗效 ,具有重要的应用价值。     

Functional and morphological aspects of Helicobacter pylori-induced gastric cancer in Mongolian gerbils

BACKGROUND: Helicobacter pylori infection of Mongolian gerbils is an established model of gastric carcinogenesis, but gastric secretory aspects of this carcinogenesis have not been studied. METHODS: The effects of single intragastric inoculation of gerbils with H. pylori strain (cagA+ vacA+, 5 x 10(6) CFU/ml) or vehicle (saline) were examined at 1, 2, 4, 6, 9, 12 and 30 weeks from inoculation. Gastric morphology, the presence of H. pylori using the rapid urease test, the density of H. pylori and 16S rRNA and the plasma gastrin and somatostatin were determined. RESULTS: H. pylori was detected in gastric mucosa in all infected animals. Basal gastric acid in gerbils was reduced by about 50% after H. pylori inoculation. Early lesions seen at 4 weeks after H. pylori inoculation consisted of chronic gastritis with thickened mucosal folds, oedema, congestion and mucosal lymphocytic infiltration. Adenomatous hyperplasia with cellular atypia with increased mitotic activity and the formation of apoptotic bodies and visible erosions and ulcerations were observed at 12-30 weeks after inoculation. The atypical gastric glands were situated 'back-to-back', suggesting gastric pre-cancer. The gastric blood flow in H. pylori-infected gerbils was significantly lower than that in the controls. Six- to seven-fold increase in plasma gastrin levels combined with significant fall in gastric somatostatin contents and the intraepithelial neoplasia were noticed in gerbils at all tested periods. CONCLUSION: H. pylori-infection in gerbils resulted in gastric pre-cancer associated with functional changes, such as suppression of gastric secretion and impairment of both gastric mucosal microcirculation and the gastrin-somatostatin link.     

Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils

BACKGROUND AND AIM: Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacter pylori (H. pylori), no studies have been conducted regarding the effect of RPZ on gastric mucosal lesion formation caused by this bacterium. In the present study, we investigated the effect of RPZ on H. pylori-associated gastric mucosal lesion formation. METHODS: Sixty-two male Mongolian gerbils were inoculated with H. pylori (ATCC43504) (Hp group) and 60 gerbils with the culture media alone (control group). Some gerbils in the Hp group and in the control group were injected with RPZ (1 mg/kg/day, for 7 days) at the 5th week. Gerbils were evaluated at the 12th, 24th and 48th weeks. RESULTS: In the Hp group, all gerbils were persistently infected for 24 weeks, but 36% became negative for H. pylori at the 48th week. In the Hp + RPZ group, 18% of gerbils at the 12th week, 40% at the 24th week, and 80% at the 48th week, became negative for H. pylori. The level of neutrophil infiltration was significantly decreased in the Hp + RPZ group in comparison to the Hp group, possibly through the effects of RPZ on initial bacterial colonization and resultant inflammation. Even in the gerbils that became H. pylori-negative, the level of neutrophil infiltration was lower in the Hp + RPZ group than in the Hp group. RPZ treatment significantly increased the level of the reduced form of glutathione (GSH) at the 48th week. The elevated levels of the reduced form of GSH may have been reduced by an antioxidation process in the H. pylori-positive Hp + RPZ group. CONCLUSION: Administration of RPZ not only inhibited gastric H. pylori colonization, but also reduced gastric mucosal inflammation in gerbils, possibly through its antibacterial action as well as pharmacological recruitment of the reduced form of GSH.     

Effects of Helicobacter pylori infection on gastric acid secretion and serum gastrin levels in Mongolian gerbils

BACKGROUND AND AIMS: Body gastritis caused by Helicobacter pylori infection appears to inhibit gastric acid secretion. The aim of this study was to determine the effects of H pylori infection on gastric acid secretion and clarify its mechanisms with reference to interleukin 1beta (IL-1beta). METHODS: (1) Mongolian gerbils were inoculated orally with H pylori. Before, six, and 12 weeks after inoculation, serum gastrin levels, gastric acid output, and IL-1beta mRNA levels in the gastric mucosa were determined. Pathological changes were also determined according to the updated Sydney system. (2) Effects of recombinant human IL-1 receptor antagonist (rhIL-1ra) on gastric acid output and serum gastrin levels were also determined. RESULTS: (1) Scores for activity and inflammation of gastritis and serum gastrin levels were significantly increased, and gastric acid output was significantly decreased six and 12 weeks after inoculation with H pylori. IL-1beta mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation with H pylori. (2) Acid output and serum gastrin levels in the infected groups returned to control levels after rhIL-1ra injection. CONCLUSIONS: Gastric acid secretion is decreased and serum gastrin levels are increased in Mongolian gerbils infected with H pylori. This change in gastric acid secretion appears to be mediated by IL-1beta induced by H pylori infection.     

蒙古沙鼠感染幽门螺杆菌后的胃部病理学变化研究

目的　建立幽门螺杆菌 (Helicobacterpylori,Hp)的蒙古沙鼠长期感染模型并观察其胃内的病理学改变。 方法　蒙古沙鼠 (8周龄 ) 80只 ,随机分为实验组 (40只 )和对照组 (40只 ) ,所有沙鼠禁食水 1d ,第 2天灌喂 5 0 %的乙醇 0 3ml,试验组第 3天及第 4天分 3次灌喂cagA Hp菌液 (10 9cfu/ml) ,0 5ml/只·次 ,对照组灌喂相同量无菌肉汤。最后一次灌喂后 2h进食水。距最后一次灌菌后 4、8、12、2 0、2 4周分别剖杀动物 ,每次实验组、对照组各 8只 ,进行微生物学检查 (粘膜涂片染色镜检、分离培养、快速尿素酶试验 )、血清学检查 (ELISA测抗Hp抗体 )和病理学检查。结果　实验组沙鼠在不同时间Hp感染率均达到 10 0 %。从第 4周开始 ,可见所有实验组沙鼠胃组织中有大量炎性细胞浸润 ,随着时间推移形成淋巴滤泡。部分沙鼠在第 12周后至 2 4周可见明显出血、慢性活动性胃炎及溃疡 ,有的溃疡可深达肌层。对照组沙鼠均无Hp定植及组织学病变。结论　蒙古沙鼠感染Hp后 ,可出现与人极相似的病理组织学改变 ,对于研究Hp的致病机制及疫苗具有重要价值     

Development of gastric adenocarcinoma in Mongolian gerbils after long-term infection with Helicobacter pylori

BACKGROUND AND AIM: The experimental evidence that long-term colonization of Helicobacter pylori results in the development of gastric cancer in Mongolian gerbils has been reported only by two Japanese groups to date. This study aimed to investigate the carcinogenicity of H. pylori infection in a Mongolian gerbil model. METHODS: Thirty-six Mongolian gerbils (inner Mongolian origin) were divided into two groups (male to female ratio, 1:1) and orally inoculated with a standard H. pylori strain (ATCC43504) or H. pylori161 (isolated from a Chinese patient with gastric adenocarcinoma), respectively, once a week for 5 weeks. Another 10 control gerbils were given phosphate-buffered saline. The animals were killed 8, 20, 28 and 84 weeks after inoculation for bacterial and histological examination. RESULTS: Seven inoculated gerbils died at the week 42. Overall, H. pylori colonization was detected in 24 (83%) of the 29 available inoculated gerbils. The gastric lesions were aggravated gradually over time. At week 84, moderate to severe gastritis, characterized by diffuse infiltration of mononuclear cells and formation of multiple lymphoid follicles in mucosa and submucosa, and even the lymphoepithelial lesions, were observed. Epithelial hyperplasia were dominant in almost all gerbils. Four (24%) of the 17 animals had hyperplastic polyps. Intestinal metaplasia were rarely seen (in three gerbils). Well-differentiated gastric adenocarcinomas developed in three (18%) of the 17 gerbils after 84 weeks. Of the three gerbils, one female gerbil was infected with H. pylori161 and the others (one male and one female) were infected with ATCC43504. CONCLUSIONS: The present study reconfirms that H. pylori infection alone can induce gastric adenocarcinoma in Mongolian gerbils and suggests that different species of gerbil and both standard and clinically isolated H. pylori strains can be used for investigating the carcinogenesis of H. pylori. This is the first report of the development of gastric cancer in female gerbils, which highlights the importance of using both sexes to investigate the pathogenesis of H. pylori and whether host susceptibility is influenced by sex.     

Anti-Helicobacter pylori therapy significantly reduces Helicobacter pylori -induced gastric mucosal damage in Mongolian gerbils

AIM: To investigate the effectiveness of 4 d‘anti-Helicobacter pyloritherapy on the H pylori-infected Mongolian gerbils based on physiological and pathological changes. METHODS: We used 6-wk-old male gerbils orally inoculated with H pylori (ATCC43504, 2&#215;10^8 CFU/mL). Seven weeks alter Hpyloriinoculation, the animals of study group received 4 d‘arti-H pyloritriple therapy (Hpylorieradicated group). Seven days later, all animals of the H pylori-eradicated and control groups (H pylori-infected &amp; H pylori-uninfected groups) were sacrificed. We examined gastric mucosal lesions macroscopically, studied gastritis microscopically and determined the stomach weight ratio, myeloperoxidase (MPO) activity and prostaglandin (PG) E2 level. RESULTS: The results showed that both macroscopic and histological gastric damages were significantly less in H pylori-eradicated group than H pylori-infected group. Stomach weight ratio, MPO activity and PGE2 levels were significantly higher in H pylori-infected group than those in the other two groups. CONCLUSION: Four days‘anti-H pylori therapy was effective in the improvement of H pylori-induced gastric lesions in Mongolian gerbils.     

Duodenogastric reflux and Helicobacter pylori infection synergistically increase gastric mucosal cell proliferative activity in Mongolian gerbils

BACKGROUND: Helicobacter pylori and duodenogastric reflux (DGR) are both recognized as aetiological factors in chronic gastritis and gastric carcinogenesis. In this study, a Mongolian gerbil (MG) model was used to investigate the histopathological changes in the gastric mucosa resulting from DGR and/or H. pylori infection. METHODS: One-hundred-and-eleven 7-week-old, specific-pathogen-free, male MGs were divided into four groups: normal controls, gerbils with surgically induced DGR, and H. pylori-infected gerbils with and without DGR. Gerbils were killed 4, 12 and 26 weeks after DGR surgery, their stomachs removed and sections prepared. Sections were fixed immediately in 20% phosphate-buffered formalin and subjected to haematoxylin and eosin staining, Alcian blue at pH 2.5/periodic acid-Schiff staining, and immunostaining for smooth muscle cells, H. pylori and 5'-bromo-2'-deoxyuridine (BrdU). RESULTS: The gastric mucosa of H. pylori-infected gerbils showed chronic active gastritis irrespective of DGR throughout the experimental period. The gastric mucosa of H. pylori-infected gerbils with DGR demonstrated higher BrdU labelling than in the other groups. CONCLUSIONS: In MGs, DGR and H. pylori infection synergistically increased gastric mucosal cell proliferative activity. DGR and H. pylori infection may be involved synergistically in gastric carcinogenesis by increasing cell proliferative activity.     

Helicobacter pylori infection induces duodenitis and superficial duodenal ulcer in Mongolian gerbils

BACKGROUND: There is no direct evidence for an animal model of Helicobacter pylori induced duodenal ulcer. AIM: In this study we evaluated the roles of bacterial strain and age of experimental animals in induction of duodenitis and duodenal ulcer in Mongolian gerbils after H pylori infection. METHODS: Specific pathogen free Mongolian gerbils were inoculated orally with three bacterial strains (H pylori ATCC 43504, TN2GF4, and K-6, a clinical isolate from a patient with gastric cancer in our clinic). These strains have both the cagA gene and VacA. Five week old gerbils were used to emulate prematurity infection and 14 week old animals were used as mature test subjects. Animals were observed for 12 weeks after inoculation. Interleukin 8 (IL-8) production in gastric epithelial cells (MKN74) after coculture with the H pylori strains was measured by ELISA. RESULTS: Gastritis and gastric ulcers were found in all gerbils infected with the three strains. However, duodenitis and gastric metaplasia were seen more frequently in gerbils infected with TN2GF4 and K-6 strains than in the ATCC 43504 infected or control groups (p<0.05). Superficial duodenal ulcers with severe duodenitis and gastric metaplasia were found in two gerbils inoculated at 14 weeks with the TN2GF4 strain but none at five weeks. The TN2GF4 strain stimulated significantly higher levels of IL-8 than ATCC 43504 and K6 strains (p=0.0039). CONCLUSIONS: When injected into adult Mongolian gerbils, a specific strain (TN2GF4) of H pylori can induce duodenitis with gastric metaplasia and superficial duodenal ulcers. Induction of duodenal ulcer in an animal model fulfills the requirements of Koch's postulates for establishing a role for H pylori as a causative agent.     

Helicobacter pylori infection potentiates aspirin induced gastric mucosal injury in Mongolian gerbils

BACKGROUND: Helicobacter pylori infection and non-steroidal anti-inflammatory drugs are two major causes of gastric ulceration but interactions between H pylori and these drugs in gastric mucosal injury are unclear. AIMS: We studied the influence of experimental H pylori infection on gastric mucosal injury induced by aspirin. SUBJECTS: Male Mongolian gerbils free of specific pathogens were used. METHODS: H pylori ATCC43504 culture broth was administered by oral gavage at seven weeks of age. After three weeks, acidified aspirin (400 mg/kg) was administered orally, and three hours later the total area of gastric erosions, myeloperoxidase (MPO) activity (an index of neutrophil accumulation), thiobarbituric acid reactive substances (TBARS, an index of lipid peroxidation), and KC/GRO (a chemoattractive cytokine in rodents) were measured in gastric mucosa. To determine the role of neutrophils in these circumstances, antigerbil neutrophil rabbit serum (ANS) was administered to some animals 18 hours before aspirin. RESULTS: Aspirin caused more extensive haemorrhagic erosions (33.1 (12.3) mm2) associated with greater MPO activity (1887.7 (598.5) microU/mg protein) and TBARS (0.33 (0.14) nmol/mg protein) and KC/GRO concentrations (28.3 (9.5) pg/mg protein) in infected than in uninfected gerbils (13.7 (2.3); 204.0 (68.9); 0.12 (0.06); 3.1 (0.8), respectively) Pretreatment with ANS inhibited the increases in gastric erosions, MPO activity, and TBARS but not KC/GRO concentration. The reduction in aspirin induced mucosal injury by administration of ANS was much greater in H pylori infected animals (65%) than in uninfected animals (31%). CONCLUSIONS: H pylori infection potentiates aspirin induced gastric mucosal injury by mechanisms that include accumulation of activated neutrophils.     

幽门螺杆菌长期感染蒙古沙土鼠腺胃模型的建立及评价

目的 建立幽门螺杆菌（Helicobacter pylori,Hp）长期感染蒙古沙土鼠腺胃模型,验证该模型出现的病理改变及腺胃肿瘤的发生情况。方法 采用国际标准菌株NCTC 11637灌喂蒙古沙土鼠,建立HP长期感染蒙古沙土鼠腺胃模型。结果 成功建立了HP长期感染蒙古沙土鼠腺胃模型,其胃黏膜的组织学变化显示,HP感染可致正常胃黏膜→慢性胃炎→萎缩→肠化生→异型增生的发展过程,Hp NCTC 11637定植于蒙古沙土鼠腺胃65财哩,可引起胃黏膜出现严重的萎缩、肠化生及不典型增生等胃癌前状态,暂未发现早期癌。结论 Hp NCTC 11637易长期定植于蒙古沙土鼠腺胃,模型的稳定性及重复性极佳,且与Hp感染人胃黏膜后出现的各种病理变化极为相似。     

Long-term treatment with sterigmatocystin,a fungus toxin,enhances the development of intestinal metaplasia of gastric mucosa in Helicobacter pylori-infected Mongolian gerbils

BACKGROUND: Helicobacter pylori is a human gastric carcinogen. Sterigmatocystin (ST), a fungus toxin, is a risk factor of gastric cancer. Cytotoxin-vacuolation toxin A (VacA) present in supernatants of H. pylori suspensions can cause gastritis and ulcer. The aim of this study was to examine the effects of H. pylori, ST and VacA in Mongolian gerbils. METHODS: Male Mongolian gerbils (n = 196) were treated with H. pylori supernatants (10 ml/1000 mg) mixed with diet or inoculated intragastrically with H. pylori alone or with ST (100 or 1000 ppb), and then killed 27 months later. Gastric tissue sections were stained with haematoxylin and eosin (H&E), periodic acid-Schiff (PAS), Alcian blue (AB, pH 2.5) and with immunostaining for PCNA and p53 expression. RESULTS: In H. pylori-infected gerbils, the normal mucosa was replaced by hyperplastic epithelium. Severe gastritis, cystic dilatation of gastric glands, hyperplastic polyps and intestinal metaplasia were observed. In H. pylori + ST (1000 ppb) gerbils, intestinal metaplasia was significantly more frequent than in H. pylori alone animals. No pathological changes were observed in the H. pylori supernatant group. Osseous metaplasia was observed in the H. pylori + ST (100 ppb) group. Serum gastrin levels of the H. pylori + ST (1000 ppb) group were significantly higher than those of the other groups. PCNA labelling index and p53 index of infected gerbils were significantly higher than those of uninfected groups. CONCLUSION: H. pylori causes gastritis, ulcer and intestinal metaplasia. ST enhances the development of intestinal metaplasia and increases gastrin levels in H. pylori-infected Mongolian gerbils.     

Establishment of Helicobacter pylori infection model in Mongolian gerbils

AIM：To establish a stable and reliable model of Helicobacter pyloriinfection model in Mongolian gerbils and to observe pathological changes in gastric mucosa in infected animals.METHODS:Mongolian gerbils were randomly divided into 18 groups;6 groups were infected with Hpylori clinical strain Y06 (n=6, groups Y), 6 groups were infected with Hpylori strain NCTC11637 (n=6, roups N),and 6 uninfected groups as negative controls (n=4,groups C).Hpylori suspensions at the concentrations of 2&#215;10^8 and 2&#215;10^9CFU/mL of strain NCTC11637 and strain Y06 were prepared. The animals in three groups N and in three groups Y were orally challenged once with 0.5 mL of the low concentration of the bacterial suspension.The animals in another three groups N and in another three groups Y were orally challenged with 0.5mL of the high concentration of the bacterial suspension for 3 times at the intervals of 24 h,respectively.For the negative controls,the animals in six groups C were orally given with the same volume of Brucella broth at the corresponding inoculating time.The animals were killed after 2nd, 4^th and 6^th week after the last challenge and the gastric mucosal specimens were taken for urease test,bacterial isolation, pathological and immunohistochemical examinations.RESULTS:Positive isolation rates of Hpyloriin the animals of groups Y at the 2nd, 4^th and 6^th week after one challenge were 0%, 16.7% and 66.7%, while in the animals of groups N were 0%, 0% and 16.7%, respectively.Positive isolation rates of Hpyloriin the animals of groups Y at the 2nd, 4^th and 6^th week after three challenges were 66.7%,100% and 100%,while in the animals of groups N were 66.7%,66.7% and 100%, respectively. In animals with positive isolation of Hpylori, the bacterium was found to colonized on the surface of gastric mucosal cells and in the gastric pits,and the gastric mucosal lamina propria was infiltrated with inflammatory cells.CONCLUSION:By using H pylori suspension at high concentration of 2&#215;10^9 CFU/mL for multiple times,the orally challenged Mongolian gerbils can be used as a stable and reliable H pylori infection model.The 2 strains of H pylori can colonize in gastric mucosa of the infected animals and cause mild inflammation reaction.     

Overexpression of cyclin E in Mongolian gerbil With Helicobacter pylori—induced gastric precancerosis

AIM: To explore dysregulation of cyclin E in malignancies,and to further investigate the role of cyclin E in Helicobacterpylori ( H. pylori)-induced gastric precancerosis.METHODS: Four-week-old specific pathogen-free maleMongolian gerbils were employed in the study. 0.5 mL 1 ×108 cfu@ L- 1 suspension of H. pylori NTCC11637 in Brucellabroth was inoculated orally into each of 20 Mongolian gerbils, and a further 20 gerbils were inoculated with Brucella brothas controls. 10 of the infected gerbils and 10 of the non-infected control gerbils were sacrificed at 25, 45 wk afterinfection. The expression of cyclin E was analyzed by RT-PCR and immunohistochemical studies with monoclonalantibody to cyclin E in Mongolian gerbil of H. pylori-induced gastric precancerosis.RESULTS: H. pylori was constantly detected in all infectedanimals throughout the study. At 25 wk after infection of H.pylori, ulcers were observed in the antral and body ofstomach ( n = 6). Histological examination showed that allanimals developed severe inflammation and multifocallymphoid follicles appeared in the lamina propria andsubmucosa of gastric antrum. At 45 wk after infection of H.pylori, severe atrophic gastritis (n = 10), intestinalmetaplasia (n = 8) and dysplasia (n = 6) could beobserved. Cyclin E mRNA levels were significantly more at25 wk after infection of H. pylori (1.27±0.26), and at45 wkafter infection of H. pylori (1.82 ± 0.39 ) than control-animals (0.59 ± 0.20, P＜ 0.01) ; cyclin E mRNA levels wereevaluated by 2.2-fold at 25 wk ( P ＜ 0.01 ) and 3. 1-fold at 45wk ( P ＜ 0.01 ) precancarosis induced by H. pylori, whencompared with control gastric epithelium of Mongoliangerbil. Immunohistochemical staining revealed exclusivenuclear staining of cyclin E. Furthermore, there wes asequential increase in cyclin E positive cells from normalepithelium to precancerosis.CONCLUSION: Overexpression of cyclin E occurs relativelyearly in gastric tumorigenesis in this model.     

Comparative Analysis of Colonization of Helicobacter pylori and Glycolipids Receptor Density in Mongolian Gerbils and Mice

The Mongolian gerbil has been used as an excellent experimental animal model for studying Helicobacter pylori infection because it can stably colonize and induce severe chronic gastritis, ulceration, and cancer-simulating human diseases in this animal. In contrast, H. pylori can only induce mild inflammation in many mouse models. The aim in this study is to clarify the difference of induction of pathological lesions in the two animal models. SPF ICR mice and Mongolian gerbils were inoculated with a clinically isolated strain of H. pylori. Six weeks after inoculation, bacteria colonizing the stomach were counted. Immunohistochemical staining and biochemical analyses of three putative receptor glycolipids were performed with monoclonal antibodies to the respective glycolipids. Significantly higher numbers of H. pylori were recovered from the stomachs of Mongolian gerbils than mice (5.77 ± 0.46 log CFU vs 4.17 ± 0.55 log CFU, P < 0.01). Immunohistochemical studies showed that sulfatide expression in the gastric mucosa of Mongolian gerbils was much stronger than that in mice, whereas the expression of Lewis^b glycolipid and GM3 were almost equal. Quantitative analysis of each glycolipid by thin-layer chromatography confirmed the results of immunohistochemical study, showing 4.1 times higher sulfatide content in the Mongolian gerbil stomach. The content of both Lewis^b and GM3 was almost equivalent in these two animals. In conclusions, higher levels of sulfatide expression, a putative adhesion receptor, in the gastric mucosa of Mongolian gerbils may allow abundant colonization by H. pylori, resulting in the development of gastric lesions in this animal model.     

Suppressive effect of rice extract on Helicobacter pylori infection in a Mongolian gerbil model

Background Rice extract has been shown to protect gastric mucosa from stress-induced damage. In this study, the antibiotic effect and the anti-inflammatory effect of orally administered aqueous rice extract on Helicobacter pylori infection and H. pylori-induced gastritis, respectively, in Mongolian gerbils were investigated.Methods Fifty specific-pathogen-free male Mongolian gerbils, seven weeks old, were divided into four groups: uninfected, untreated animals (group A); uninfected, rice extract-treated animals (group B); H. pylori-infected, untreated animals (group C); and H. pylori-infected, rice extract-treated animals (group D). Group C and D animals were killed 12 weeks after H. pylori infection (i.e., at 19 weeks of age) and group A and B animals were also killed at age 19 weeks. The stomachs were removed for histopathological examination with hematoxylin-and-eosin staining and anti-5-bromo-2-deoxyuridine (BrdU) immunostaining, and to determine the bacterial burden. Serum anti-H. pylori antibody titers were also tested.Results In groups A and B, the gastric mucosa showed no inflammatory cell infiltration and a few BrdU-reactive cells. Group C animals developed marked chronic active gastritis in the gastric mucosa, and BrdU-labeled cells in the gastric mucosa markedly increased in number. In group D animals, a significant reduction occurred in the degree of neutrophilic polymorphonuclear cell infiltration into the gastric mucosa, in the BrdU-labeling indices of gastric epithelial cells, and in anti-H. pylori antibody titers in the serum (P < 0.01), compared with although H. pylori was not completely eradicated.Conclusions The rice extract was effective in suppressing inflammation and epithelial cell proliferation in the gastric mucosa in H. pylori-infected Mongolian gerbils. The rice extract has potential to exhibit a protective effect on H. pylori-related gastric mucosal diseases.     

蒙古沙土鼠不同幽门螺杆菌菌株感染相关性胃病的研究进展

幽门螺杆菌(Helicobacter pylori,H.pylori)感染在世界范围内高发,他定植于人胃黏膜,导致慢性胃炎及胃癌的发生.蒙古沙鼠(mongolian gerbil,MG)很少患自发性胃炎,且不是H.pylori 的自然宿主.人工接种H.pylori后,蒙古沙鼠患H.pylori相关性胃病与胃病患者最相似...     

Quantitative measurement of nitric oxide and hydrogen peroxide in Helicobacter pylori-infected Mongolian gerbils in vivo

OBJECTIVE: Peroxynitrite formation, as reflected by nitrotyrosine expression, is low in Helicobacter pylori-infected Mongolian gerbils despite pronounced expression of radical-forming enzymes. The aim of the present study was to investigate in vivo whether H. pylori inhibits either one or both of the nitro- and oxyradical formation pathways. MATERIAL AND METHODS: Male Mongolian gerbils were infected with two different H. pylori strains, TN2GF4 and SS1. Six months after inoculation, direct measurement of NO and H2O2 was performed in vivo using electrochemical microsensors positioned in close proximity to the gastric mucosa. RESULTS: In the TN2GF4-infected animals the level of NO was significantly lower than that in controls. No significant difference in NO levels was detected between the SS1-infected group and the controls. H2O2 was significantly increased in the SS1 animals compared with that in controls after 6 months. The H2O2 level in the TN2GF4 group did not differ from that in controls. CONCLUSIONS: The results indicate that H. pylori infection is associated with strain-dependent functional inhibition of both the NO and oxyradical formation pathways in the gastric mucosa.