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

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*

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*

OBJECTIVETo study the therapeutic mechanism of weitongning (WTN) in treating peptic ulcer.

METHODSRat model of chronic gastric ulcer induced by glacial acetic acid was used to observe the effect of WTN on the curative quality, thickness of regenerated mucous membrane, epidermal growth factor (EGF) and nitric oxide (NO) contents in scar tissue around the gastric ulcer.

RESULTSThe thickness of regenerated mucous membrane, EGF and NO contents in peri-ulcer scar tissue were higher in the model rats after WTN treatment than that in the untreated model rats (P<0.01 or P<0.05).

CONCLUSIONWTN could elevate the quality of ulcer curing, to raise the EGF and NO contents in peri-ulcer scar tissue might be one of its mechanisms for preventing relapse of peptic ulcer.

Animals ; Anti-Ulcer Agents ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Epidermal Growth Factor ; metabolism ; Female ; Gastric Mucosa ; metabolism ; Male ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stomach ; metabolism ; Stomach Ulcer ; metabolism

AIMTo investigate the effects of sodium sulfonate daidzein (SSD) on stress-induced gastric ulcer and explore its possible mechanism.

METHODSUsing exhausted swimming and counting the number of gastric ulcer to establish the model of stress-induced gastric ulcer. Mouse experience intraperitoneal injection of different doses of SSD and L-NAME, and NDP histochemical method was used to detect the changes of nitric oxide synthase (NOS) positive neurons in stomach.

RESULTSSSD had dose-dependent protective effect on gastric mucosa. L-NAME could prevent stress induced gastric lesion. After combined injection of L-NAME and effective dose of SSD, the protective effect of SSD on gastric mucosa was reinforced. The number of NOS ganglion was constant, and effective dose of SSD had slight effect on NOS-positive neurons in normal mouse while it decreased NOS positive neurons in per area and in per ganglia after stress.

CONCLUSIONThe increased nitric oxide (NO) leads to gastric ulcer during stress, SSD has protective effect on gastric mucosa and this effect may be mediated by inhibiting NOS and restricting the overproduction of NO during stress.

Animals ; Gastric Mucosa ; drug effects ; pathology ; Isoflavones ; pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Nitric Oxide ; metabolism ; Stomach Ulcer ; Stress, Physiological

OBJECTIVETo investigate the ulcer-preventive effect of bismuth glycyrrhizate on experimental gastric ulcer and its mechanisms.

METHODThree kinds of model animals with experimental gastric ulcer were established and gastric mucosal injuries were induced by pyloric ligation in rats, applying ethanol in rats and imposing stress in mice, respectively. The rats were divided into experimental groups treated with bismuth glycyrrhizat 700, 350, 175 mg kg(-1), positive control group treated with cimetidine (200 mg kg(-1), and negative control group treated with 0.1% EDTA. The mice were divided into experimental groups treated with bismuth glycyrrhiza 980, 490, 250 mg kg(-1). The gastric ulcer index, gastric juice volume, acidity, pepsin activity, the level of nitric oxide (NO) in serum and the level of prostaglandin E2 in gastric tissue were measured in rats.

RESULTBismuth glycyrrhizate was shown to be able to reduce the gastric juice volume, acidity and pepsin activity as well as gastric ulcer index. It could increase the content of NO in serum and the content of prostaglandin E2 in gastric tissue.

CONCLUSIONThe bismuth glycyrrhizate has antiulcer effect in rats.

Animals ; Anti-Ulcer Agents ; pharmacology ; Bismuth ; pharmacology ; Dinoprostone ; metabolism ; Female ; Gastric Mucosa ; metabolism ; pathology ; Glycyrrhizic Acid ; pharmacology ; Male ; Mice ; Nitric Oxide ; blood ; Pepsin A ; metabolism ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; metabolism ; pathology

OBJECTIVETo study the antiulcer effects and the mechanism of Veronicastrum axillare (Sieb. et Zucc) Yamazaki (VAY) on ethanol induced gastric ulcer rats.

METHODSTotally 48 healthy SD rats were randomly divided into 6 groups, i.e., the normal group, the model group, the ranitidine group, the high dose VAY group, the medium dose VAY group, and the low dose VAY group, 8 in each group. Rats in the normal group and the model group were administered with normal saline respectively. Rats in the ranitidine group were administered with 0.18% ranitidine suspension (at the daily dose of 0.027 g/kg) by gastrogavage. Those in the high dose VAY group, the medium dose VAY group, and the low dose VAY group were administered with VAY at the daily dose of 2.8 g/kg, 1.4 g/kg, and 0.7 g/kg by gastrogavage, once daily for 14 consecutive days. The gastric ulcer model was established using absolute ethanol after the last gastrogavage. The ulcer index and the ulcer inhibitory rate were compared. The concentrations of malonyldialdehyde (MDA), nitric oxide (NO), epidermal growth factor (EGF), and the activity of superoxide dismutase (SOD) in the serum and the homogenate of the gastric mucosa tissue were detected.

RESULTSCompared with the model group, the gastric ulcer index in the rest groups obviously decreased (P < 0.01). The ulcer index was dose-dependent with VAY (P < 0.01), with the highest gastric ulcer index shown in the high dose VAY group (P < 0.01). Compared with the normal group, the concentrations of MDA and NO significantly increased in the serum and the gastric mucosa tissue, the activity of SOD and the EGF content in the gastric mucosa tissue of rats in the model group significantly decreased (P < 0.01). Compared with the model group, the MDA concentrations in the serum and the gastric mucosa tissue decreased, the serum NO content increased, the NO content in the gastric mucosa tissue decreased, the serum SOD activity increased, the EGF content in the gastric mucosa tissue increased in the rest groups, all showing statistical difference (P < 0.05, P < 0.01).

CONCLUSIONSThe water extract of VAY had significant effects on ethanol induced gastric ulcer. Its mechanisms might lie in reducing the generation of free radicals, promoting the oxygen free radical clearance, restraining lipid peroxidation, regulating and controlling the in vivo contents of NO and EGF.

Animals ; Anti-Ulcer Agents ; pharmacology ; therapeutic use ; Epidermal Growth Factor ; metabolism ; Ethanol ; adverse effects ; Male ; Malondialdehyde ; metabolism ; Plant Extracts ; pharmacology ; therapeutic use ; Plantago ; chemistry ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; drug therapy ; etiology ; metabolism ; Superoxide Dismutase ; metabolism

OBJECTIVETo explore relevant material basis of moxibustion for recovering gastric mucosal lesion. METHODL Forty-five SD rats were randomly divided into a normal goup, a model group, an acupoint group and a control group, 15 rats in the model group and 10 rats in the rest three groups. Except the normal group, binding and cold stress method were used to establish gastric mucosa injury model. The suspended moxibustion was applied in the acupoint group and control group at acupoints of the stomach meridian ("Liangmen" (ST 21) and "Zusanli" (ST36) and control acupoints (Laterally 1cm next to the "Liangmen" (ST 21) and Zusanli" (ST36), once a day, consectutively for 12 days. After 12 days, morphology of gastric mucosal was observed under optical microscope; protein fingerprints of gastric mucosa cell in rats were detected by protein fingerprint technology, weak cation chip and weak anion chip. Also mass to charge ratio of differential proteins in groups were compared and analyzed.

RESULTSCompared with the model group, index of gastric mucosal lesion in the acupoint group was reduced and its morphology was obviously improved (P<0.05). Campared with control group, index and morphology of gastric mucosal lesion were significantly improved in the acupoint group (P<0.05). According to test of weak cation chip, there was four marker proteins that had expression differences, indicating moxibustion at acupoints of stomach meridian could inrease expression of three marker protein whose molecular weight was 1354Da, 5692Da and 8432Da (all P<0.05) while reduce expression of marker protein with molecular weight of 3287Da (_<0.05). According to test of weak anion chip, moxibustion at acupoints of stomach meridian could increase expression of three marker proteins whose molecular weight was 2412 Da, 3026Da and 6475 Da (allP<0.05).

CONCLUSIONMoxibustion at acupoints of the stomach meridian could regulate differential expression of gastric mucosa cell-related marker protein in rats with acute gastric ulcer and recover gastric mucosal lesion, it's effect is better than that of the points of laterally 1 cm next to acupoint.

Acupuncture Points ; Animals ; Female ; Gastric Mucosa ; metabolism ; Humans ; Male ; Moxibustion ; Proteins ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; genetics ; metabolism ; therapy

OBJECTIVETo investigate the role of the change in glucocorticoid receptor in stress-induced gastric ulcer in severely burned rats.

METHODSWistar rats inflicted with 30% TBSA full-thickness burn were employed as the model. The dynamic postburn change in the glucocorticoid receptor in gastric mucosal tissue and gastric mucosal injury (injury index) were observed.

RESULTSThe gastric mucosal cortisol content increased as of 3 postburn hours (PBHs) and peaked at 12 PBHs. But the cytoplasmic glucocorticoid receptor content in the gastric mucosal cells decreased evidently. In addition, the gastric mucosal injury index increased obviously at 12 and 24 PBHs.

CONCLUSIONThe decrease of gastric mucosal cytoplasmic glucocorticoid receptor content might be closely related to the stress-induced gastric mucosal injury.

Animals ; Burns ; complications ; metabolism ; Disease Models, Animal ; Male ; Rats ; Rats, Wistar ; Receptors, Glucocorticoid ; metabolism ; physiology ; Stomach Ulcer ; complications ; metabolism ; Stress, Physiological ; complications

Gastric cancer is one of the most common cancers worldwide. The purpose of this study was to find out potential markers for gastric cancer. Tumor and normal tissues from 152 gastric cancer cases were analyzed by two-dimensional gel electrophoresis (2-DE). The images of silver stained gels were analyzed and statistical analysis of spot intensities revealed that spot 4262 showed higher expression (5.7-fold increase) in cancer tissues than in normal tissues (P< 0.001). It was identified by peptide mass fingerprinting as nicotinamide N-methyltransferase (NNMT). A monoclonal antibody with a detection limit down to 10 ng was produced against NNMT in mouse. Using the prepared monoclonal antibody, western blot analysis of NNMT was performed for gastric tissues from 15 gastric cancer patients and two gastric ulcer patients. The results corroborated those of 2-DE experiments. A single spot was detected in gastric ulcer tissues while four to five spots were detected in gastric cancer tissues. In cancer tissues, two additional spots of acidic and basic form were mainly detected on 2-DE gels. This suggests that NNMT receives a post-translational modification in cancer- specific manner.
Tumor Markers, Biological/isolation & purification ; Tissue Distribution ; Stomach Ulcer/metabolism ; Stomach Neoplasms/*metabolism ; Proteome/analysis ; *Protein Processing, Post-Translational ; Phosphorylation ; Nicotinamide N-Methyltransferase/immunology/*metabolism ; Mice, Inbred BALB C ; Mice ; Humans ; Carcinoma/*metabolism ; Blotting, Western/methods ; Antibodies, Monoclonal/biosynthesis ; Animals