Helicobacter pylori infection alters gastric microbiota structure and biological functions in patients with gastric ulcer or duodenal ulcer

BACKGROUND Helicobacter pylori(H.pylori)infection is closely associated with gastrointestinal diseases.Our preliminary studies have indicated that H.pylori infection had a significant impact on the mucosal microbiome structure in patients with gastric ulcer(GU)or duodenal ulcer(DU).AIM To investigate the contributions of H.pylori infection and the mucosal microbiome to the pathogenesis and progression of ulcerative diseases.METHODS Patients with H.pylori infection and either GU or DU,and healthy individuals without H.pylori infection were included.Gastric or duodenal mucosal samples was obtained and subjected to metagenomic sequencing.The compositions of the microbial communities and their metabolic functions in the mucosal tissues were analyzed.RESULTS Compared with that in the healthy individuals,the gastric mucosal microbiota in the H.pylori-positive patients with GU was dominated by H.pylori,with signi-ficantly reduced biodiversity.The intergroup differential functions,which were enriched in the H.pylori-positive GU patients,were all derived from H.pylori,particularly those concerning transfer RNA queuosine-modification and the synthesis of demethylmenaquinones or menaquinones.A significant enrichment of the uibE gene was detected in the synthesis pathway.There was no significant difference in microbial diversity between the H.pylori-positive DU patients and healthy controls.CONCLUSION H.pylori infection significantly alters the gastric microbiota structure,diversity,and biological functions,which may be important contributing factors for GU.

Perforated gastric ulcer causing mediastinal emphysema: A case report

BACKGROUND Mediastinal emphysema is a condition in which air enters the mediastinum between the connective tissue spaces within the pleura for a variety of reasons.It can be spontaneous or secondary to chest trauma,esophageal perforation,medi-cally induced factors,etc.Its common symptoms are chest pain,tightness in the chest,and respiratory distress.Most mediastinal emphysema patients have mild symptoms,but severe mediastinal emphysema can cause respiratory and circulatory failure,resulting in serious consequences.CASE SUMMARY A 75-year-old man,living alone,presented with sudden onset of severe epigastric pain with chest tightness after drinking alcohol.Due to the remoteness of his residence and lack of neighbors,the patient was found by his nephew and brought to the hospital the next morning after the disease onset.Computed tomography(CT)showed free gas in the abdominal cavity,mediastinal emph-ysema,and subcutaneous pneumothorax.Upper gastrointestinal angiography showed that the esophageal mucosa was intact and the gastric antrum was perforated.Therefore,we chose to perform open gastric perforation repair on the patient under thoracic epidural anesthesia combined with intravenous anesthesia.An operative incision of the muscle layer of the patient's abdominal wall was made,and a large amount of subperitoneal gas was revealed.And a continued incision of the peritoneum revealed the presence of a perforation of approx-imately 0.5 cm in the gastric antrum,which we repaired after pathological examination.Postoperatively,the patient received high-flow oxygen and cough exercises.Chest CT was performed on the first and sixth postoperative days,and the mediastinal and subcutaneous gas was gradually reduced.CONCLUSION After gastric perforation,a large amount of free gas in the abdominal cavity can reach the mediastinum through the loose connective tissue at the esophageal hiatus of the diaphragm,and upper gastrointestinal angiography can clarify the site of perforation.In patients with mediastinal emphysema,open surgery avoids the elevation of the diaphragm caused by pneumoperitoneum compared to laparoscopic surgery and avoids increasing the mediastinal pressure.In addition,thoracic epidural anesthesia combined with intravenous anesthesia also avoids pressure on the mediastinum from mechanical ventilation.

Tilapia Head Glycolipid Alleviates Indomethacin-Induced Gastric Ulcer via Regulating Oxidative Stress and Inflammation Through COX/PGE2 Signaling Pathway in Adult Rats

The aim of this experiment was to investigate the ameliorative effect and molecular mechanism of tilapia head glycolipid(TH-GL)on indomethacin(IDM)-induced gastric ulcer in male Sprague Dawley(SD)rats.The gastric ulcer model was established by oral administration of 30mgkg^(-1) IDM after 7 days of TH-GL or omeprazole(OME)administration in rats.Then the macroscopic gastric injury symptoms,gastric mucosa protective factor cyclooxygenase 1(COX-1),cyclooxygenase 2(COX-2),prostaglandin E_(2)(PGE_(2)),the levels of oxidative stress,and inflammatory cytokine expression levels in the rats were analyzed.The experimental results showed that multiple ulcers appeared on the gastric surface of the rats in the model group.Compared to the model group,TH-GL significantly alleviated gastric ulcers and reduced the gastric damage index in rats.In addition,TH-GL significantly promoted the expression of constitutive enzyme COX-1 while inhibited the expression of inducible enzyme COX-2,and make PGE2 maintain at normal levels.TH-GL also inhibited oxidative stress and inflammatory responses,increased superoxide dismutase(SOD)activity and glutathione(GSH)content,decreased the level of malondialdehyde(MDA)and the content of pro-inflammatory factor.In conclusion,these results suggested that TH-GL could maintain the expression levels of COX-1 and PGE2 while inhibit the expression of COX-2 in the gastric of rat and then prevent IDM-induced gastric ulcer,which may be related to the regulation of oxidative stress and inflammatory response.Therefore,TH-GL might be a new option for the prevention of gastric diseases induced by IDM.

Albizzia chinensis(Osbeck)Merr extract YS ameliorates ethanol-induced acute gastric ulcer injury in rats by regulating NRF2 signaling pathway

Background:Around the world,there is a high incidence of gastric ulcers.YS,an extract from the Chinese herb Albizzia chinensis(Osbeck)Merr,has potential therapeutic applications for gastrointestinal diseases.Here we elucidated the protective effect and underlying mechanism of action of YS on gastric ulcer in rats injured by ethanol.Methods:The ethanol-i nduced gastric ulcer rat model was used to assess the protective effect of YS.A pathological examination of gastric tissue was performed by H&E staining.GES-1 cells damaged by hydrogen peroxide were used to simulate oxidative damage in gastric mucosal epithelial cells.Endogenous NRF2 was knocked down using small interfering RNA.Immunoprecipitation was used to detect ubiquitination of NRF2.Co-i mmunoprecipitation was used to detect the NRF2-Keap1 interaction.Results:YS(10 and 30 mg/kg,i.g.)significantly reduced the ulcer index,decreased MDA level,and increased SOD and GSH levels in gastric tissues damaged by ethanol.YS promoted NRF2 translocation from cytoplasm to nucleus and enhanced the NQO1 and HO-1 expression levels in injured rat gastric tissue.In addition,YS regulated NQO1 and HO-1 via NRF2 in H_(2)O_(2)-i nduced oxidative injured GES-1 cells.Further studies on the underlying mechanism indicated that YS reduced the interaction between NRF2 and Keap1 and decreased ubiquitylation of NRF2,thereby increasing its stability and expression of downstream factors.NRF2 knockdown abolished the effect of YS on MDA and SOD in GES-1 cells treated with H_(2)O_(2).Conclusion:YS reduced the NRF2-Keap1 interaction,promoting NRF2 translocation into the nucleus,which increasing the transcription and translation of NQO1 and HO-1 and improved the antioxidant capacity of rat stomach.

Influence of a diet meal plan on pepsinogen I and II,gastrin-17,and nutritional status in gastric ulcer patients

BACKGROUND Gastric ulcers(GUs)have a high risk of clinical morbidity and recurrence,and further exploration is needed for the prevention,diagnosis,and treatment of the disease.AIM To investigated the effects of a diet plan on pepsinogen(PG)I,PG II,gastrin-17(G-17)levels and nutritional status in patients with GUs.METHODS A total of 100 patients with GUs treated between May 2022 and May 2023 were enrolled,with 47 patients in the control group receiving routine nursing and 53 patients in the experimental group receiving dietary nursing intervention based on a diet plan.The study compared the two groups in terms of nursing efficacy,adverse events(vomiting,acid reflux,and celialgia),time to symptom improvement(burning sensation,acid reflux,and celialgia),gastric function(PG I,PG II,and G-17 levels),and nutritional status[prealbumin(PA)and albumin(ALB)levels].RESULTS The experimental group showed a markedly higher total effective rate of nursing,a significantly lower incidence of adverse events,and a shorter time to symptom improvement than the control group.Additionally,the experimental group’s post-intervention PG I,PG II,and G-17 levels were significantly lower than preintervention or control group levels,whereas PA and ALB levels were significantly higher.CONCLUSION The diet plan significantly reduced PG I,PG II,and G-17 levels in patients with GUs and significantly improved their nutritional status.

Sequential bowel necrosis and large gastric ulcer in a patient with a ruptured femoral artery:A case report

BACKGROUND Severe bleeding as a result of a major vascular injury is a potentially fatal event commonly observed in the emergency department.Bowel necrosis and gastric ulcers secondary to ischemia are rare due to their rich blood supply.In this case,we present the case of a patient who was treated successfully following rupture of his femoral artery resulting in bowel necrosis and an unusually large gastric ulcer.CASE SUMMARY A 28-year-old male patient sustained a knife stab wound to the right thigh,causing rupture of his femoral artery and leading to massive bleeding.He underwent cardiopulmonary resuscitation and received a large blood transfusion.Abdominal surgeries confirmed bowel necrosis,and jejunostomy was performed.The necrotic intestine was removed,the remaining intestine was anastomosed,and the right thigh was amputated.After three surgeries,the patient's overall condition gradually improved,and the patient was discharged from the hospital.However,one day after discharge,the patient was admitted again due to dizziness and melena,and a gastroduodenoscopy revealed a giant banded ulcer.After 2 weeks of treatment,the ulcer had decreased in size without bleeding.Six months after the last surgery,enterostomy and reintroduction surgery were completed.The patient was fitted with a right lower limb prosthesis one year after surgery.After 3 years of follow-up,the patient did not complain of discomfort.CONCLUSION Trauma department physicians need to be aware of the possible serious complications involving the abdomen of trauma patients with massive bleeding.

Endoscopic treatment of bleeding gastric ulcer causing gastric wall necrosis:A case report

BACKGROUND Gastric wall necrosis is a rare complication of endoscopic treatment for bleeding gastric ulcer,which may exacerbate the patient’s condition once it occurs and may even require surgical intervention for treatment.CASE SUMMARY A 59-year-old man was admitted to our department with melena.Endoscopy revealed a giant ulcer in the gastric antrum with a visible vessel in its center,which was treated with sclerosants and tissue glue injection and resulted in necrosis of the gastric wall.CONCLUSION Injection of sclerosants and tissue glue may lead to gastric wall necrosis,which is a serious complication.Therefore,before administering this treatment to patients,we should consider other more effective methods of hemostasis to avoid gastric wall necrosis.

Progress of Research on the Effect of Dietary Care on Patients with Gastritis and Gastric Ulcers

Gastritis gastric ulcer is a common disease of the digestive system,which has a serious impact on the quality of life and health of affected individuals.Dietary care is one of the important measures to treat and prevent gastritis gastric ulcers.This paper reviews the research progress on the impact of dietary care on patients with gastritis and gastric ulcers,including dietary behavioral intervention,dietary habit cultivation,dietary hygiene education,and nutritional support.Studies have shown that rational dietary care was able to improve the clinical symptoms of patients,regulate the intestinal microbial community,anti-inflammatory,antioxidant,and other pathways to improve the pathophysiological state of patients with gastritis and gastric ulcer and prevent recurrence.Therefore,dietary care is of great significance to patients with gastritis and gastric ulcers.

History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer

Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis). Gastric and duodenal ulcers and gastric cancer have been known for thousands of years. Ulcers are generally non-fatal and until the 20th century were difficult to diagnose. However, the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present. It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century. Here, we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern, as it proved to be when it could be examined directly in the late 19th century. The environment before the 20th century favored acquisition of H. pylori infection and atrophic gastritis (e.g., poor sanitation and standards of living, seasonal diets poor in fresh fruits and vegetables, especially in winter, vitamin deficiencies, and frequent febrile infections in childhood). The latter part of the 19th century saw improvements in standards of living, sanitation, and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent. In the early 20th century physician’s believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for “surgical disease” or for “Sippy” diets. We show that while H. pylori remained common and virulent in Europe and the United States, environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H. pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H. pylori-related diseases.

Effects of Aloe vera and sucralfate on gastric microcirculatory changes,cytokine levels and gastric ulcer healing in rats

AIM： To compare the effects of Aloe vera and sucralfate on gastric microcirculatory changes, cytokine levels and gastric ulcer healing. METHODS： Male Spraque-Dawley rats （n=48） were divided into four groups. Group 1 served as control group, group 2 as gastric ulcer group without treatment, groups 3 and 4 as gastric ulcer treatment groups with sucralfate and Aloe vera. The rats from each group were divided into 2 subgroups for study of leukocyte adherence, TNF-α and IL-10 levels and gastric ulcer healing on days 1 and 8 after induction of gastric ulcer by 20% acetic acid. RESULTS： On day 1 after induction of gastric ulcer, the leukocyte adherence in postcapillary venule was significantly （P〈 0.05） increased in the ulcer groups when compared to the control group. The level of TNF-α was elevated and the level of IL-10 was reduced. In the ulcer groups treated with sucralfate and Aloe vera, leukocyte adherence was reduced in postcapillary venule. The level of IL-10 was elevated, but the level of TNF-a had no significant difference. On day 8, the leukocyte adherence in postcapillary venule and the level of TNF-α were still increased and the level of IL-10 was reduced in the ulcer group without treatment. The ulcer treated with sucralfate and Aloe vera had lower leukocyte adherence in postcapillary venule and TNF-α level. The level of IL-10 was still elevated compared to the ulcer group without treatment. Furthermore, histopathological examination of stomach on days 1 and 8 after induction of gastric ulcer showed that gastric tissue was damaged with inflammation. In the ulcer groups treated with sucralfate and Aloe vera on days 1 and 8, gastric inflammation was reduced, epithelial cell proliferation was enhanced and gastric glands became elongated. The ulcer sizes were also reduced compared to the ulcer group without treatment. CONCLUSION： Administration of 20% acetic acid can induce gastric inflammation, increase leukocyte adherence in postcapillary venule and TNF-α level and reduce IL-10 level. Aloe vera treatment can reduce leukocyte adherence and TNF-αlevel, elevate IL-10 level and promote gastric ulcer healing.

Refractory gastric ulcer with abundant IgG4-positive plasma cell infiltration: A case report

We describe a 77-year-old man with refractory gastric ulcer that worsened after Helicobacter pylori eradication therapy.Pathology showed marked infiltration of IgG4-positive plasma cells in the gastric lesions,which led us to suspect IgG4-related sclerosing disease.To the best of our knowledge,this is the first report of IgG4-related gastric ulcer without the main manifestation of autoimmune pancreatitis.

Effects of hydrotalcite combined with esomeprazole on gastric ulcer healing quality: A clinical observation study

AIM To evaluate the effects of hydrotalcite combined with esomeprazole on gastric ulcer healing quality. METHODS Forty-eight patients diagnosed with gastric ulcer between June 2014 and February 2016 were randomly allocated to the combination therapy group or monotherapy group. The former received hydrotalcite combined with esomeprazole, and the latter received esomeprazole alone, for 8 wk. Twenty-four healthy volunteers were recruited and acted as the healthy control group. Endoscopic ulcer healing was observed using white light endoscopy and narrow band imaging magnifying endoscopy. The composition of collagen fibers, amount of collagen deposition, expression of factor. and TGF-beta 1, and hydroxyproline content were analyzed by Masson staining, immunohistochemistry, immunofluorescent imaging and ELISA. RESULTS Following treatment, changes in the gastric microvascular network were statistically different between the combination therapy group and the monotherapy group (P < 0.05). There were significant differences (P < 0.05) in collagen deposition, expression level of Factor. and TGF-beta 1, and hydroxyproline content in the two treatment groups compared with the healthy control group. These parameters in the combination therapy group were significantly higher than in the monotherapy group (P < 0.05). The ratio of collagen. to collagen. was statistically different among the three groups, and was significantly higher in the combination therapy group than in the monotherapy group (P < 0.05). CONCLUSION Hydrotalcite combined with esomeprazole is superior to esomeprazole alone in improving gastric ulcer healing quality in terms of improving microvascular morphology, degree of structure maturity and function of regenerated mucosa.

Mechanisms of action of leptin in preventing gastric ulcer

To investigate the effects of leptin （1-20μg/kg） on acidified ethanol （AE）- and indomethacin （Indo）-induced gastric lesions in rats and compare it with ranitidine, lansoprazole, and omeprazole and to determine its mechanisms of actions.METHODS： Gastric ulcers, which were approximately 1 mm in width, formed in the glandular portion of the gastric mucosa produced by oral administration of either AE or Indo were taken as ulcer index. The inhibitory effect of subcutaneous administration of leptin, two proton pump inhibitors （PPIs） lansoprazole and omeprazole, or H2-receptor antagonist ranitidine 30 min before AE or Indo was evaluated.A radioimmunoassay was used to determine the PGE2 concentration in the homogenate of the glandular portion of the stomach. We performed histological study of the glandular stomach for the evaluation of total, acidic, and sulfated mucus content.RESULTS： Subcutaneous administration of leptin, two PPI slansoprazole and omeprazole or H2-receptor antagonist ranitidine 30 min before AE or Indo produced a dosedependent and reproducible inhibition of gastric ulcers （GUs）. This inhibition was found to be more potent than other antagonists used. In N^G-nitro L-arginine methyl ester （L-NAME）-pretreated animals, the ulcer prevention ability of leptin in AE-induced ulcer was significantly reduced,compared to rats without L-NAME pretreatment. However,the ulcer prevention ability of leptin was not altered by L-NAME treatment in Indo-induced ulcers. Leptin produced a dose-dependent increase in PGE2 level in the gastric glandular tissues. Leptin also increased mucus secretion.CONCLUSION： The results of the present study show that leptin inhibits GU formation by AE or Indo in a dosedependent and reproducible manner in rats. The results also suggest that leptin prevents ulcer formation by increasing the activities of the cyclo-oxygenase and/or nitric oxide pathways and by increasing mucus secretion.

Aqueous suspension of anise “Pimpinella anisum” protects rats against chemically induced gastric ulcers

AIM： To substantiate the claims of Unani and Arabian traditional medicine practitioners on the gastroprotective potential effect of a popular spice anise, ＂Pimpinella anisum L.＂ on experimentally-induced gastric ulceration and secretion in rats. METHODS： Acute gastric ulceration in rats was produced by various noxious chemicals including 80% ethanol, 0.2 mol/L NaOH, 25% NaCI and indomethacin. Anti-secretory studies were undertaken using pylorusligated Shay rat technique. Levels of gastric non-protein sulfhydryls （NP-SH） and wall mucus were estimated and gastric tissue was also examined histologically. Anise aqueous suspension was used in two doses （250 and 500 mg/kg body weight） in all experiments. RESULTS： Anise significantly inhibited gastric mu- cosal damage induced by necrotizing agents and indomethacin. The anti-ulcer effect was further confirmed histologically. In pylorus-ligated Shay rats, anise suspension significantly reduced the basal gastric acid secretion, acidity and completely inhibited the rumenal ulceration. On the other hand, the suspension significantly replenished ethanol-induced depleted levels of gastric mucosal NP-SH and gastric wall mucus concentration. CONCLUSION： Anise aqueous suspension possesses significant cytoprotective and anti-ulcer activities against experimentallynduced gastric lesions. The anti-ulcer effect of anise is possibly prostaglandin-mediated and/orthrough its anti-secretory and antioxidative properties.

Genetic alterations in benign lesions:Chronic gastritis and gastric ulcer

AIM： To investigate the occurrence of chromosome 3, 7, 8, 9, and 17 aneuploidies, TPS3 gene deletion and p53 protein expression in chronic gastritis, atrophic gastritis and gastric ulcer, and their association with H pylori infection. METHODS： Gastric biopsies from normal mucosa （NM, n = 10）, chronic gastritis （CG, n = 38）, atrophic gastritis （CAG, n=13） and gastric ulcer （GU, n=21） were studied using fluorescence in situ hybridization （FISH） and immunohistochemical assay. A modified Giemsa staining technique and PCR were used to detect Hpylori. An association of the gastric pathologies and aneuploidies with Hpylori infection was assessed. RESULTS： Aneuploidies were increasingly found from CG （21%） to CAG （31%） and to GU （62%）, involving mainly monosomy and trisomy 7, trisomies 7 and 8, and trisomies 7, 8 and 17, respectively. A significant association was found between H pylori infection and aneuploidies in CAG （P=0.0143） and GU （P=0.0498）. No TP53 deletion was found in these gastric lesions, but p53-positive immunoreactivity was detected in 45% （5/11） and 12% （2/17） of CG and GU cases, respectively. However, there was no significant association between p53 expression and H pylori infection. CONCLUSION： The occurrence of aneuploidies in benign lesions evidences chromosomal instability in early stages of gastric carcinogenesis associated with Hpylori infection, which may confer proliferative advantage. The increase of p53 protein expression in CG and GU may be due to overproduction of the wild-type protein related to an inflammatory response in mucosa.

Protective effects of Ginkgo biloba extract on the ethanol-induced gastric ulcer in rats

AIM: To evaluate the preventive effect of Ginkgo biloba extract (GbE) on ethanol-induced gastric mucosal injuries in rats. METHODS: Female Wistar albino rats were used for the studies. We randomly divided the rats for each study into five subgroups: normal control, experimental control, and three experimental groups. The gastric ulcers were induced by instilling 1 mL 50% ethanol into the stomach. We gave GbE 8.75,17.5,26.25 mg/kg intravenously to the experimental groups respectively 30 min prior to the ulcerative challenge. We removed the stomachs 45 min later. The gastric ulcers, gastric mucus and the content of non-protein sulfhydryl groups (NP-SH), malondialdehyde (MDA), c-Jun kinase (JNK) activity in gastric mucosa were evaluated. The amount of gastric juice and its acidity were also measured. RESULTS: The findings of our study are as follows: (1) GbE pretreatment was found to provide a dose-dependent protection against the ethanol-induced gastric ulcers in rats; (2) the GbE pretreatment afforded a dose-dependent inhibition of ethanol-induced depletion of stomach wall mucus, NP-SH contents and increase in the lipid peroxidation (increase MDA) in gastric tissue; (3) gastric ulcer induced by ethanol produced an increase in JNK activity in gastric mucosa which also significantly inhibited by pretreatment with GbE; and (4) GbE alone had no inhibitory effect on gastric secretion in pylorus-ligated rats. CONCLUSION: The finding of this study showed that GbE significantly inhibited the ethanol-induced gastric lesions in rats. We suggest that the preventive effect of GbE may be mediated through: (1) inhibition of lipid peroxidation; (2) preservation of gastric mucus and NP-SH; and (3) blockade of cell apoptosis.

Effect of Jianweiyuyang granule on gastric ulcer recurrence and expression of VEGF mRNA in the healing process of gastric ulcer in rats

AIM: To investigate the effect of Jianweiyuyang (JWYY)granule on gastric ulcer recurrence and its mechanism in the treatment of gastric ulcer in rats.METHODS: Gastric ulcer in rats was induced according to Okeba's method with minor modification and the recurrence model was induced by IL-1β. The expression of vascular endothelial growth factor mRNA (VEGF mRNA) was examined by reverse transcription polymerase chain reaction in gastric ulcer and microvessel density (MVD) adjacent to the ulcer margin was examined by immunohistochemistry.RESULTS: MVD was higher in the JWYY treatment group (14.0±2.62) compared with the normal, model and ranitidine treatment groups (2.2±0.84, 8.8±0.97, 10.4±0.97) in rats (P＜0.01). The expression level of VEGF mRNA in gastric tissues during the healing process of JWYY treatment group rats significantly increased compared with other groups (normal group: 0.190±0.019, model group: 0.642±0.034,ranitidine group: 0.790±0.037, P＜0.01).CONCLUSION: JWYY granules can stimulate angiogenesis and enhance the expression of VEGF mRNA in gastric ulcer rats. This might be the mechanism for JWYY accelerating the ulcer healing, and preventing the recurrence of gastric ulcer.

Protective role of metallothionein in stress-induced gastric ulcer in rats

AIM: To illustrate the pathophysiological role of metallothionein (MT) in gastric ulcer induced by stress. METHODS: Wistar rats underwent water-immersionrestraint (WIR) stress, ZnSO4 (an MT inducer) treatment, WIR+ZnSO4 or WIR+MT, and the ulcer index (UI) was estimated in excised stomach and liver tissues. The mRNA level of gastric MT was determined by semi-quantitative RT-PCR. The MT content in gastric and hepatic tissues was determined by Cd/hemoglobin affinity assay. The lipid peroxidation products malondialdehyde (MDA) and conjugated dienes (CD) were estimated by use of thiobarbituric acid reactive species and ultraviolet spectrophotometry. RESULTS: WIR stress induced severe gastric mucosal lesions in rats. Compared with control rats, stressed rats had increased lipid peroxide content in serum and stomach and liver tissues. MDA content was increased by 34%, 21% and 29% and CD level by 270%, 83% and 28%, respectively. MT content in the stomach and liver was increased by 0.74- and 1.8-fold, and the MT-mRNA level in the stomach was increased by 26%. Pretreatment with ZnSO4 prevented gastric lesion development (the UI was 87% lower than that without pretreatment), and the MDA and CD content in serum and tissues was lower. The MT content in the liver was double in rats that were not pretreated, and the MT mRNA level in the stomach was 35% higher. MT administration 1 h before the WIR stress prevented gastric lesion development (the UI decreased by 47% compared with that in rats not pretreated), and the MDA and CD content in serum and tissues was significantly lower. CONCLUSION: In WIR-stressed rats, the MT level was increased in serum and in stomach and liver tissues. Pre-administration of exogenous MT or pre-induction of endogenous MT can protect the gastric mucosa against stress-induced ulcers and inhibits the formation of stressinduced lipid peroxide. MT could have a gastroprotective effect and might be a new interventive and therapeutic target in stress-induced gastric ulcers.

Quality of gastric ulcer healing evaluated by endoscopic ultrasonography

AIM: To evaluate the quality of gastric ulcer healing after different antiulcer treatment by endoscopic ultrasonography(EUS).METHODS: The patients were divided into three groups, and received lansoprazole, amoxicillin and clarithromycinfor 1 wk. Then group A took lansoprazole combined with tepreton for 5 wk, group B took lansoprazole and group C took tepreton for 5 wk. Endoscopy and EUS were performed before and 6 wk after medication. RESULTS: There was no significant difference in cumulative healing rate to S stage between the groups (89%, 82%vs83%,P＞0.05). The rate of white scar formation was significantly higher in group A than in groups B and C (67%, 36%, 50%, P＜0.05). The average contraction rates of the width of ulcer crater, length of disrupted muscularis propria layer and hypoechoic area were higher in groupA than in groups B and C (0.792±0.090, 0.660±0.105 vs0.668±0.143, P＜0.05). The hypoechoic area disappeared in four cases of group A, one of group B and two of group C. The percentage of hypoechoic area disappearance was higher in group A than in the other two groups (44%, 9%vs 17%, P＜0.05). Gastric ulcer healing was better ingroup A.CONCLUSION: The combined administration of proton pump inhibitors and mucosal protective agent can improve gastric ulcer healing.

Comparison of He/icobacter py/ori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pyloriinfection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites.METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylineosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation,glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System.RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%,respectively) were significantly higher than those in 4 102chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%,and 37.0%, respectively, P＜0.05). The rate of H pylori colonization of chronic gastritis in ＜30 years, 31-40 years,41-50 years, 51-60 years, 61-70 years and ＞70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%,50.7%, 43.5%, respectively; in corpus, it was 32.6%,41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%,43.5%, respectively. The rate of Hpyloricolonization of gastric ulcer in ＜30 years, 31-40 years, 41-50 years,51-60 years, 61-70 years and ＞70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%,respectively; in corpus, it was 59.7%, 79.6%, 83.6%,80.1%, 70.6%, 59.1%, respectively; in angulus, it was61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%,respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below50 years, with chronic gastritis and in patients, below40 years, with gastric ulcer. In the other age- groups,the rate of H pylori colonization was highest in corpus,lower in antrum and lowest in angulus (all P＜0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P＜0.01). In comparison of gastric ulcer patients with chronic gastritis patients,the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis(both P＜0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P＜0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P＜0.01).CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.