Although our present knowledge of the etiology of peptic ulcer is incomplete, the presence or absence of peptic ulcer is determined by the delicate interplay between aggressive factors (secreted gastric acid and pepsin) and defensive factors (mucosal resistance). Peptic ulcer is produced when the aggressive effects of acid-pepsin dominate the protective effects of gastric or duodenal mucosal resistance by predominance of aggressive factors or interruption of defensive factors. KU-54 enhances mucosal resistance to tissue injury by the increase of gastric mucosal blood flow, the stimulation of gastric mucosal metabolism, the increase of glycoprotein of gastric mucus, and the increase of ATP of gastric mucosa. We have treated 38 cases of gastric ulcers with KU-54 300 mg daily for 4-12 weeks for the evaluation of the therapeutic efficacy. Endoscopic, clinical, and laboratory assessments were undergone before and after 4 ~ 12 weeks of the treatment. Major symptoms of gastric ulcer have been improved in 83.3% after the medication with KU-54. The healing rate of gastric ulcer evaluated by endoscopy was observed in 33.3% after 4 weeks, 73.3% after 8 weeks, 76.6% after 12 weeks of the medication with KU-54. The utility rate of KU-54 was 86.7%. We could conclude that KU-54 is the utilizable drug for gastric ulcer.
Adenosine Triphosphate ; Endoscopy ; Gastric Acid ; Gastric Mucosa ; Glycoproteins ; Metabolism ; Mucus ; Peptic Ulcer ; Stomach Ulcer*

OBJECTIVETo explore a method which can remove the gastric mucus in order to prepare mucous membrane single cell suspension for the research of cytomics.

METHODSEnzymology was used to remove the mucus gel and to separate mucous layer from the normal fresh gastric tissue. The mucous layer was broken to prepare single cell suspension with machine method. Expression of major cyclins in mucous layer cells was examined by cytoimmunochemistry, flow cytometry(FCM) and confocal microscopy.

RESULTSThe 0.1% pepsin could dissolve the mucus gel and 1.2-2.4 U/L dispase could separate the mucous layer completely. The single mucous cell suspension was prepared successfully. FCM results from mucous single cell suspension revealed that expression of cyclin D(3), B(1) was obvious, that of cyclin D(2) was weak and that of cyclin D(1), A, E was the least. Similar results were found with confocal microscopy.

CONCLUSIONSSingle cell suspension from mucous layer can be easily prepared by pepsin and dispase. Cyclins schedule expression in vivo is different from cyclins schedule expression in vitro.

Cell Line ; Cell Proliferation ; Cyclins ; metabolism ; Flow Cytometry ; Gastric Mucins ; metabolism ; Gastric Mucosa ; cytology ; metabolism ; Humans ; Mucous Membrane ; cytology ; metabolism

Animals ; Chickens ; Cold Temperature ; adverse effects ; Gastric Mucosa ; metabolism ; pathology ; physiopathology ; Intestinal Mucosa ; metabolism ; pathology ; physiopathology ; Male ; Serum ; metabolism

Mucins,a family of heavily glycosylated proteins,present mainly in epithelial cells.They function as essential barriers for epithelium and play important roles in cellular physiological processes.Aberrant expression and glycosylation of mucins in gastric epithelium occur at pathological conditions,such as Helicobacter pylori infection,chronic atrophic gastritis,intestinal metastasis,dysplasia,and gastric cancer.This review addresses the major roles played by mucins and associated O-glycan structures in normal gastric epithelium.Further,we expound the alterations of expression patterns and glycan signatures of mucins at those pathological conditions.
Gastric Mucosa/pathology* ; Glycosylation ; Helicobacter Infections/pathology* ; Helicobacter pylori/metabolism* ; Humans ; Mucins/metabolism* ; Stomach Neoplasms/pathology*

OBJECTIVETo investigate effects of electroacupuncture on gastric mucosal intestinal trefoil factor (ITF) gene expression in the rat of gastric mucosal injury induced by stress.

METHODSForty rats were randomly divided into 4 groups: blank group, model group, stomach channel group, gallbladder channel group. The normal group did not receive any processing, and the model group were fixed for 7 sessions and both the stomach channel group and the gallbladder channel group received 7 sessions of electro-acupuncture before modeling. The model was made by water restraint stress (WRS) for 10 hours. Index of gastric mucosal injury was detected and then the gastric mucosa tissue in each rat was taken and the expression of ITFmRNA of the tissue was detected by the reverse transcriptase-polymerase chain reaction (RT-PCR) method.

RESULTSThere was very significant or significant difference in the gastric mucosal injury as the stomach channel group and the gallbladder channel group compared with the model group (P < 0.05 or P < 0.01); electroacupuncture had a tendency of improving the expression of gastric mucosal ITFmRNA gene; the expression of ITFmRNA in the gallbladder channel group and the stomach channel group was significantly higher than that of the model group (P < 0.05, P < 0.01).

CONCLUSIONThe special regulation of electroacupuncture on gastric mucosal tissue is related with the release of epidermal growth factor and the expression of intestinal trefoil factor gene.

Animals ; Electroacupuncture ; Gastric Mucosa ; metabolism ; Gene Expression ; RNA, Messenger ; genetics ; Rats ; Stomach Diseases ; Stomach Ulcer ; metabolism

Acetylcholine ; pharmacology ; Adenocarcinoma ; metabolism ; Cell Line, Tumor ; Gastric Mucosa ; cytology ; drug effects ; metabolism ; Humans ; Receptors, Cholinergic ; metabolism ; Stomach Neoplasms ; metabolism

Molecular knowledge of human gastric corpus epithelium remains incomplete. Here, by integrated analyses using single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and single-cell assay for transposase accessible chromatin sequencing (scATAC-seq) techniques, we uncovered the spatially resolved expression landscape and gene-regulatory network of human gastric corpus epithelium. Specifically, we identified a stem/progenitor cell population in the isthmus of human gastric corpus, where EGF and WNT signaling pathways were activated. Meanwhile, LGR4, but not LGR5, was responsible for the activation of WNT signaling pathway. Importantly, FABP5 and NME1 were identified and validated as crucial for both normal gastric stem/progenitor cells and gastric cancer cells. Finally, we explored the epigenetic regulation of critical genes for gastric corpus epithelium at chromatin state level, and identified several important cell-type-specific transcription factors. In summary, our work provides novel insights to systematically understand the cellular diversity and homeostasis of human gastric corpus epithelium in vivo.
Humans ; Epigenesis, Genetic ; Gastric Mucosa/metabolism* ; Chromatin/metabolism* ; Stem Cells ; Epithelium/metabolism* ; Fatty Acid-Binding Proteins/metabolism*

This study aims to identify the active components and the mechanism of Jingqi Yukui Capsules(JQYK) in the treatment of gastric ulcer based on network pharmacology, and verify some key targets and signaling pathways through animal experiment. To be specific, first, the active components and targets of JQYK were retrieved from a Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine(BATMAN-TCM) and Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP), and the targets of gastric ulcer from GeneCards and Online Mendelian Inheritance in Man(OMIM) with the search term "gastric ulcer". The common targets of the two were the potential targets of the prescription for the treatment of the di-sease. Then, protein-protein interaction(PPI) network of key targets were constructed based on STRING and Cytoscape 3.7.2, followed by Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment by matescape database and pathway visualization by Omicshare. For the animal experiment, the improved method of Okabe was used to induce gastric ulcer in rats, and the model rats were classified into the model group, JQYK high-dose(JQYK-H), medium-dose(JQYK-M), and low-dose(JQYK-L) groups, Anweiyang Capsules(WYA) group, and Rabeprazole Sodium Enteric Capsules(RBPZ) group. Normal rats were included in the blank group. Rats in the blank group and model group were given distilled water and those in the administration groups received corresponding drugs. Then gastric ulcer healing in rats was observed. The changes of the gastric histomorphology in rats were evaluated based on hematoxylin-eosin(HE) staining, and the content of inducible nitric oxide synthase(iNOS) in rat gastric tissue was detected with Coomassie brilliant blue method. The mRNA and protein levels of some proteins in rat gastric tissue were determined by real-time quantitative polymerase chain reaction(RT-qPCR) and Western blot(WB) to further validate some key targets and signaling pathways. A total of 206 active components and 535 targets of JQYK, 1 305 targets of gastric ulcer, and 166 common targets of the disease and the drug were yielded. According to PPI analysis and KEGG pathway enrichment analysis, multiple key targets, such as interleukin-6(IL-6), tumor necrosis factor(TNF), mitogen-activated protein kinase 1(MAPK1), MAPK3, and MAPK14, as well as nuclear factor kappa-B(NF-κB) signaling pathway, IL-17 signaling pathway, and leukocyte transendothelial migration in the top 20 key signaling pathways were closely related to inflammation. The key protein p38 MAPK and NF-κB signaling pathway were selected for further verification by animal experiment. The gastric ulcer in the JQYK-H group recovered nearly to the level in the blank group, with significant decrease in the content of iNOS in rat gastric tissue and significant reduction in the mRNA and phosphorylation levels of p38 MAPK and the mRNA and protein levels of NF-κB p65 in rat gastric tissue. The results indicated that JQYK can inhibit the phosphorylation of the key protein p38 MAPK and the expression of NF-κB p65 in the NF-κB signaling pathway, thereby exerting the anti-inflammatory effect and effectively improving the quality of gastric ulcer healing in rats. Thus, the animal experiment result verifies some predictions of network pharmacology.
Animal Experimentation ; Animals ; Capsules ; Gastric Mucosa/metabolism* ; Humans ; Network Pharmacology ; Rats ; Stomach Ulcer/genetics*

AIMTo demonstrate the protective effect of nitric oxide (NO) on gastric mucosa and its relationship to the acid secretion of parietal cells under stress in rats.

METHODSWater immersion-restraint stress (WRS) model in SD rats was performed. The gastric mucosal ulcer index (UI), NO contents in gastric mucosa and H+, K(+) -ATPase activity of parietal cells were measured. The effects of N(G)-nitro-L-arginine methyl ester(L-NAME) and L-arginine (L-Arg) on the H+, K(+)-ATPase activity of parietal cells and stress-induced gastric mucosal lesion were observed.

RESULTSL-NAME pretreatment decreased NO contents in gastric mucosa, activated H+, K(+) -ATPase activity of parietal cells and aggravated gastric mucosal lesion, whereas L-Arg pretreatment increased NO contents, inhibited H+, K(+) -ATPase activity and significantly ameliorated stress-induced gastric mucosal lesion.

CONCLUSIONEndogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.

Animals ; Arginine ; metabolism ; Gastric Acid ; secretion ; Gastric Mucosa ; metabolism ; H(+)-K(+)-Exchanging ATPase ; metabolism ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Oxidative Stress ; Parietal Cells, Gastric ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; metabolism ; pathology ; Stress, Physiological

OBJECTIVETo investigate the distribution patterns of neuron-specific enolase (NSE) and synaptophysin (SYN) during the development of human fetal stomach.

METHODSSixteen specimens of human fetal (gestational age 2 to 4 months) gastric tissues were examined with immunohistochemistry for detecting the distribution of NSE and SYN expressions in the gastric walls.

RESULTSDuring the second to fourth gestational months, NSE was strongly expressed in the nerve cells and nerve fibers of the myenteric nerve plexus of human fetal stomach. As the gestational age increased, the numbers of NSE positive cells and fibers increased gradually in the gastric submucosa, but NSE was negative in the gastric mucosa. At the second gestational month, SYN expression was negative in the mucosa but positive in the myenteric nerve plexus; during the third to fourth months, positive SYN expression was found in the mucosa, submucosa and myenteric nerve plexus of the embryonic gastric walls and its expression intensity increased with the gestational age.

CONCLUSIONSYN and NSE are both involved in the regulation of the nervous system in the gastric wall but their expressions and distributions follow different patterns during the development of human fetal stomach.

Fetus ; metabolism ; Gastric Mucosa ; metabolism ; Gestational Age ; Humans ; Immunohistochemistry ; Myenteric Plexus ; Nerve Fibers ; metabolism ; Neurons ; metabolism ; Phosphopyruvate Hydratase ; metabolism ; Stomach ; metabolism ; Synaptophysin ; metabolism