The aim of this study was to examine whether Helicobacter pylori (H. pylori) attaches to areas of intestinal metaplasia in Korean patients. Gastric biopsy specimens with intestinal metaplasia from 8 gastric cancers, 24 gastric ulcers, 11 duodenal ulcers, and 57 chronic gastritis were examined. The specimens were stained with periodic acid-Schiff/alcian blue pH 2.5 and high-iron diamine/alcian blue pH 2.5 to identify the subtype of intestinal metaplasia, and then immunohistochemical stain was done with rabbit anti-H. pylori polyclonal antibody. In 17 patients, H. pylori attached to areas of type II intestinal metaplasia. All areas of intestinal metaplasia showing adherence contained sialomucin, and H. pylori was not detected in the areas of intestinal absorptive cells and sulfomucin-containing metaplastic cells.
Adult ; Aged ; Bacterial Adhesion/physiology* ; Female ; Gastric Mucosa/pathology* ; Gastric Mucosa/microbiology* ; Helicobacter pylori/physiology* ; Human ; Intestines/pathology* ; Intestines/microbiology* ; Korea ; Male ; Metaplasia ; Middle Age

Helicobacter pylori (H. pylori) undergoes decades long colonization of the gastric mucosa of half the population in the world to produce acute and chronic gastritis at the beginning of infection, progressing to more severe disorders, including peptic ulcer disease and gastric cancer. Prolonged carriage of H. pylori is the most crucial factor for the pathogenesis of gastric maladies. Bacterial persistence in the gastric mucosa depends on bacterial factors as well as host factors. Herein, the host and bacterial components responsible for the incipient stages of H. pylori infection are reviewed and discussed. Bacterial adhesion and adaptation is presented to explain the persistence of H. pylori colonization in the gastric mucosa, in which bacterial evasion of host defense systems and genomic diversity are included.
Gastric Mucosa/*microbiology ; Gastritis/*microbiology/pathology ; Helicobacter Infections/*microbiology ; Helicobacter pylori/*physiology ; Humans ; Stomach Neoplasms/pathology

OBJECTIVETo evaluate the role of gastric mucosa apoptosis in the stress of ischemic stroke, and to discuss the relationship between gastric mucosa apoptosis and gastric barrier.

METHODSTen dogs were artificially made ischemic stroke by operation (IS group), and another 10 shamly-operated dogs were served as control group. Sucrose permeability were measured after the operation. All dogs were sacrificed 24 hours after operation to measure the gastric mucosal apoptosis index, gastric gross classification, and histological score.

RESULTSThe gastric mucosal apoptosis index in the IS group were significantly higher than in the control group (14.83 +/- 4.41 vs. 5.60 +/- 2.61, P < 0.05). The gastric mucosal apoptosis index were correlated with the sucrose permeability (r = 0. 89, P < 0.05) , gastric gross classification (r = 0. 87, P < 0.05), and histological score (r = 0.92, P < 0.05).

CONCLUSIONSAlthough ischemic stroke will not cause the obvious damage in the respiratory and circulatory system, it is responsible for the apoptosis of epithelial cell in the gastric mucosa and gastric barrier dysfunction. The apoptosis index is closely correlated with the damage of the function and morphology of the gastric barrier, indicating that the epithelial cell apoptosis acceleration in the gastric mucosa may result in the damage of gastric barrier function.

Animals ; Apoptosis ; physiology ; Dogs ; Epithelial Cells ; pathology ; Gastric Mucosa ; pathology ; In Situ Nick-End Labeling ; Random Allocation ; Stroke ; pathology ; physiopathology

The effect of gastric ischemia-reperfusion (GI-R) on gastric mucosal cellular apoptosis and proliferation was investigated using histological, immunohistochemical methods in Sprague-Dawley rats. The GI-R model was established by clamping the celiac artery for 30 min and reperfusing for 0, 0.5, 1, 3, 6, 24, 48, 72 h, respectively. Mild gastric mucosal injury was induced by ischemia alone. However, the injury worsened and reached the maximum at 1 h after reperfusion, almost simultaneously with the gastric mucosal cellular apoptosis increase and cellular proliferation decrease in gastric mucosa. Then, gastric mucosal cells began to repair by increasing gastric cellular proliferation, which achieved the maximum at 24 h after reperfusion. The mucosal lesions were almost completely repaired at about 72 h after reperfusion. These results indicate that the gastric mucosal injury after GI-R is mainly induced by reperfusion. The damaged gastric mucosa could initiate its repairing mechanism immediately through inhibiting cellular apoptosis and increasing the number of proliferative cells, which substitute the damaged cells gradually. The plerosis almost completes in three days after reperfusion showing a strong self-repair ability of gastric mucosa.
Animals ; Apoptosis ; physiology ; Cell Proliferation ; Female ; Gastric Mucosa ; pathology ; physiology ; Ischemia ; physiopathology ; Male ; Rats ; Rats, Sprague-Dawley ; Regeneration ; physiology ; Reperfusion Injury ; physiopathology ; Stomach ; blood supply ; pathology ; physiology

OBJECTIVETo explore the effect of bile in inducing gastric mucosal injury in rats.

METHODSSD rats were divided into 4 groups, namely bile duct ligation group, duodenogastric reflux (DGR) group, DGR plus bile duct ligation group and normal control group. The pathological changes in the gastric mucosa and tight junction 3 months after gastrojejunostomy were observed and compared with the findings in the normal control rats.

RESULTSCompared with the rats in DGR plus bile duct ligation group, the rats in DGR group showed obvious gastric mucosal hyperemia, foveolar hyperplasia and severely impaired tight junction between the gastric mucosal cells.

CONCLUSIONBile plays an important role in gastric mucosal injury due to DGR.

Animals ; Bile ; physiology ; Duodenogastric Reflux ; physiopathology ; Gap Junctions ; pathology ; Gastric Mucosa ; pathology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley

The changes on the regional distributions and frequencies of two types of chromogranin, chromogranin A (CGA) and bovine Sp-1 chromogranin (BCG)-immunoreactive (IR)cells in gastrointestinal (GI)tract of osteoporotic Sprague-Dawley rat induced by ovariectomy were studied by immunohistochemical methods. The experimental animals were divided into two groups, one is non-ovariectomized group (Sham)and the other is ovariectomized group (OVX). Samples were collected from each part of GI tract at 10th week after ovariectomy or sham operation. CGA-IR cells were restricted to the stomach regions with various frequencies regardless of ovariectomy except for the fundus of OVX in which no cells were detected. In addition, BCG-IR cells were also restricted to the pylorus and duodenum regardless of ovariectomy. A significantly decrease of CGA IR cells was detected in OVX compared to that of Sham in both fundus and pylorus, and BCG-IR cells were also significantly decreased in the duodenum(p<0. 05). However, in the pylorus, BCG-IR cells in OVX showed similar frequency compared to that of Sham. In conclusion, the abnormality in density of chromogranin, a generally used GI endocrine cell marker, detected in this study may contribute to the development of GI symptoms in osteoporosis such as impairments of calcium and some lipids, frequently encountered in patients with postmenopausal osteoporosis.
Animals ; Chromogranin A ; Chromogranins/*metabolism ; Female ; Gastric Mucosa/*metabolism/pathology ; Gene Expression Regulation/physiology ; Humans ; Immunoglobulins/*metabolism ; Immunohistochemistry ; Intestinal Mucosa/*metabolism/pathology ; Models, Animal ; Osteoporosis, Postmenopausal/*metabolism/pathology ; Ovariectomy ; Rats ; Rats, Sprague-Dawley

The present study aimed to investigate the protective effect and mechanism of hydrogen sulfide donor NaHS administration against gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) in rats. GI-R injury was induced by clamping the celiac artery of adult male SD rats for 30 min and followed by reperfusion for 1 h. The rats were randomly divided into sham group, GI-R group, NaHS group, glibenclamide group and pinacidil group. Gastric mucosal damage was analyzed with macroscopic injured area, deep damage was assessed with histopathology scores, and the hydrogen sulfide concentration in plasma was determined by colorimetric method. The results showed that pretreatment of NaHS significantly reduced the injured area and deep damage of the gastric mucosa induced by GI-R. However, NaHS did not significantly alter the levels of hydrogen sulfide in plasma 14 d after NaHS administration. The gastric protective effect of NaHS during reperfusion could be attenuated by glibenclamide, an ATP-sensitive potassium channel (K(ATP)) blocker. However, K(ATP) opener pinacidil inhibited the GI-R-induced injury. These results suggest that exogenous hydrogen sulfide plays a protective role against GI-R injury in rats possibly through modulation of K(ATP) channel opening.
Animals ; Gastric Mucosa ; pathology ; Hydrogen Sulfide ; metabolism ; Ischemic Preconditioning ; methods ; KATP Channels ; metabolism ; physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Stomach ; blood supply ; Sulfides ; pharmacology

OBJECTIVEThe aim of this study was to investigate the expression of connexin (Cx) and the function of gap junction intercellular communication (GJIC) in the carcinogenesis, progression and metastasis of gastric cancers.

METHODSImmunohistochemistry was used to detect the expression of Cx32 and Cx43 proteins in tissue samples. Indirect immunofluorescence assay was used to investigate the expression of Cx32 and Cx43 proteins in several gastric cancer lines of various differentiation grades. The expression of Cx43 in samples of gastric cancer tissue, adjacent normal tissue and in the gastric cancer cell lines of various differentiation grades was detected by Western blot. Scrape-loading dye transfer (SLDT) technique was used to detect the function of gap junction intercellular communication (GJIC) in the various cell lines.

RESULTSIn the normal gastric mucosa the expression rates of both Cx32 and Cx43 were 100%. In gastric cancers, the expression rates of Cx32 andCx43 were 49.5% (55/111) and 39.6% (44/111), respectively. There was a significant difference between their expression in normal and cancer tissues (P < 0.05). Age of the patients was not significantly correlated with the expression level of Cx32 and Cx43 (P > 0.05). Cx43 expression was significantly associated with the TMN stage, histological type, depth of infiltration and distant metastasis (P < 0.05), but Cx32 expression was not significantly correlated with depth of infiltration ( P > 0.05). In the cancer cell lines, a positive expression of Cx32 and Cx43 was detected in transfected human stomach mucosal cell line (CES-1) and human well differentiated stomach cancer cell line (N87), but negative in the poorly differentiated stomach cancer cell line (BGC-823) at all. Both Cx32 and Cx43 expression rates were 100% in the cell line GES-1. Cx32 expression rate was 49.0% and Cx43 expression rate was 55.0% in the cell line N87. But in the poorly differentiated cancer cell line BGC-823 both Cx32 and Cx43 expression was negative. GJIC function detection showed: GES-1 showed well GIJC function but no GIJC function in the cell lines N87 and BGC-823. The intensity of fluorescence was gradually decreasing from GES-1 cells to N87 cells and almost no fluorescence in BGC-823 cells. Western blotting showed that Cx43 expression in normal tissue was higher than that in gastric cancer tissue, and in the cell lines GES-1, N87 and BGC-823, the bands seemed decreasing progressively. There was very low expression in BGC-823 cells.

CONCLUSIONThe decreasing expression of connexin Cx32 and Cx43 is obviously correlated with the occurrence, development and metastatic potential of stomach cancers.

Adenocarcinoma ; metabolism ; pathology ; Adult ; Aged ; Cell Communication ; physiology ; Cell Line, Tumor ; Connexin 43 ; metabolism ; Connexins ; metabolism ; Down-Regulation ; Female ; Gap Junctions ; physiology ; Gastric Mucosa ; metabolism ; Humans ; Male ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasm Staging ; Stomach Neoplasms ; metabolism ; pathology

Restraint water-immersion stress (RWIS), a compound stress model, has been widely used to induce acute gastric ulceration in rats. A wealth of evidence suggests that the central nucleus of the amygdala (CEA) is a focal region for mediating the biological response to stress. Different stressors induce distinct alterations of neuronal activity in the CEA; however, few studies have reported the characteristics of CEA neuronal activity induced by RWIS. Therefore, we explored this issue using immunohistochemistry and in vivo extracellular single-unit recording. Our results showed that RWIS and restraint stress (RS) differentially changed the c-Fos expression and firing properties of neurons in the medial CEA. In addition, RWIS, but not RS, induced the activation of corticotropin-releasing hormone neurons in the CEA. These findings suggested that specific neuronal activation in the CEA is involved in the formation of RWIS-induced gastric ulcers. This study also provides a possible theoretical explanation for the different gastric dysfunctions induced by different stressors.
Action Potentials ; drug effects ; physiology ; Analysis of Variance ; Animals ; Central Amygdaloid Nucleus ; pathology ; Corticotropin-Releasing Hormone ; metabolism ; Disease Models, Animal ; Gastric Mucosa ; pathology ; Gene Expression Regulation ; physiology ; Neurons ; physiology ; Patch-Clamp Techniques ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats ; Rats, Wistar ; Stress, Physiological ; physiology ; Stress, Psychological ; etiology ; physiopathology

BACKGROUNDWe investigated the role in electrical stimulations of paraventricular nucleus (PVN) on gastric mucosal cells and the activity of mitogen-activated protein kinases (MAPKs) family members induced by gastric ischemia-reperfusion (GI-R). And we elucidated the molecular mechanisms of the protection of PVN from GI-R injuries.

METHODSSprague-Dawley rats were divided randomly into 4 groups: Group I, the sham-operated GI-R control group; Group II, the sham-operated electrical stimulations to PVN + sham-operated GI-R control group; Group III, the GI-R group; and Group IV, the electrical stimulations to PVN + GI-R group. In all of the experiments, the PVN was stimulated prior to the induction of GI-R. The GI-R model was established by clamping the celiac artery for 30 minutes to induce ischemia and then was released to allow reperfusion for 30 minutes, 1 hour, 3 hours and 6 hours, respectively. The gastric mucosal cellular apoptosis, proliferation, and the expression and activity of MAPKs protein were observed by immunohistochemistry and Western blotting, respectively.

RESULTSCompared with the GI-R group, the application of electrical stimulations in the PVN significantly depressed gastric mucosal cellular apoptosis and enhanced gastric mucosal cellular proliferation following the 30-minute, 1-hour and 3-hour intervals of reperfusion; it also promoted the activation of p-ERK during the early phase of reperfusion but inhibited the activation of p-JNK1/2 and p-p38 following the 30-minute, 1-hour and 3-hour intervals of reperfusion.

CONCLUSIONSThe protection of PVN against GI-R injuries may attribute to the inhibition of apoptosis and the promotion of the proliferation of gastric mucosal cells during GI-R. This protective effect is mediated by activating the ERK pathway and depressing the JNK, p38 MAPK pathways of the gastric mucosal cells.

Animals ; Apoptosis ; Cell Proliferation ; Electric Stimulation ; Extracellular Signal-Regulated MAP Kinases ; physiology ; Gastric Mucosa ; blood supply ; enzymology ; pathology ; JNK Mitogen-Activated Protein Kinases ; physiology ; MAP Kinase Signaling System ; physiology ; Male ; Paraventricular Hypothalamic Nucleus ; physiology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; p38 Mitogen-Activated Protein Kinases ; physiology