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

Acetylcholine ; pharmacology ; Cell Line, Tumor ; Cell Membrane ; Epithelial Cells ; cytology ; Gastric Mucosa ; cytology ; drug effects ; metabolism ; Humans ; Receptors, Nicotinic ; drug effects ; metabolism ; Stomach Neoplasms ; 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

AIM AND METHODSBy hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and a high dose of capsaicin to ablate the capsaicin-sensitive afferent fibers, the roles of capsaicin-sensitive afferent fibers and endogenous NO in the gastric acid secretion and hyperemic response to intragastric distention were studied in rats.

RESULTS(1) There was an increase in acid secretion associated with the increase in GMBF to intragastric distention. (2) Pretreatment with a high dose of capsaicin to ablate afferent fibers completely abolished the GMBF and partially inhibited the acid secretion during the intragastric distention. (3) The increase in GMBF to intragastric distention was completely blocked by pretreatment with L-NAME, whereas the acid secretion was significantly attenuated.

CONCLUSIONCapsaicin-sensitive afferent fibers and endogenous NO are involved in the increases of gastric acid secretion and GMBF.

Animals ; Capsaicin ; pharmacology ; Gastric Acid ; secretion ; Gastric Dilatation ; metabolism ; Gastric Juice ; secretion ; Gastric Mucosa ; blood supply ; Male ; NG-Nitroarginine Methyl Ester ; Neurons, Afferent ; drug effects ; Nitric Oxide ; physiology ; Rats ; Rats, Sprague-Dawley

AIMTo study the influence of acetylcholine (ACh) on nicotinic receptor(N receptor) beta-subunit of the gastric epithelia and the gastric adenocarcinoma cells, and the difference of both cells.

METHODSImmunohistochemistry method was used to examine the number, number density and surface density of N receptor beta-subunit in both cells cultured in vitro.

RESULTSThe number and number density of N receptor beta-subunit in the gastric adenocarcinoma cells were much more than that in the gastric epithelia (P < 0.05). But surface density of N receptor beta-subunit in the gastric adenocarcinoma cells were lower than that in the gastric epithelia (P < 0.05). ACh at 10(6) mol/L could increase the number, number density and surface density of N receptor beta-subunit in the gastric epithelia (P < 0.01). The increase effect could not be blocked by atropine. ACh had no effect on N receptor beta-subunit in the gastric adenocarcinoma cells.

CONCLUSIONACh at low concentration initiates N receptor desensitization in the gastric epithelia. ACh has no effect on sensitivity of N receptor beta-subunit in the gastric adenocarcinoma cells.

Acetylcholine ; pharmacology ; Adenocarcinoma ; metabolism ; Cells, Cultured ; Epithelial Cells ; drug effects ; Gastric Mucosa ; cytology ; Humans ; Receptors, Nicotinic ; metabolism ; Stomach Neoplasms ; metabolism ; Tumor Cells, Cultured

BACKGROUNDSericin peptide (SP) has shown a powerful anti-oxidant property in a host of studies. The present study was designed to investigate the possible protective effects of SP against alcohol-induced gastric lesions in mice and to explore the potential mechanisms.

METHODSAnimals were randomly divided into 5 groups: control, alcohol (56%, 14.2 ml/kg), SP-treated mice (0.2, 0.4, 0.8 g/kg). Mice were pretreated with SP before administering alcohol, the concentration of ethanol in serum and urine, the contents of malondialdehyde (MDA), glutathione (GSH) and the glutathione peroxidase (GSH-PX), catalase (CAT) and superoxide dismutase (SOD) activities in the gastric mucosa were measured, subsequently, the pathological evaluation of stomach was also observed.

RESULTSOf the animals pre-treated with SP (0.4, 0.8 g/kg), the concentration of ethanol in serum was significantly decreased, while increased in urine as compared to the alcohol-administered alone animals. Alcohol administration caused severe gastric damage as indicated by markedly increased MDA levels and decreased antioxidants, such as reduced GSH, GSH-PX and SOD in the gastric tissue while the CAT activity was not altered. On SP administration there was a reversal in these values towards normal. Histopathological studies confirmed the beneficial role of SP, which was in accordance with the biochemical parameters.

CONCLUSIONSSP could protect gastric mucosa from alcohol-induced mucosal injury. These gastroprotective effects might be due to increasing 'first-pass metabolism' in the stomach and hastening ethanol elimination directly through the urine. SP might also play an important role in the protection of the structure and function of gastric mitochondria, at least partly based on their anti-oxidant effect.

Amino Acids ; analysis ; Animals ; Cytoprotection ; Ethanol ; blood ; toxicity ; urine ; Gastric Mucosa ; drug effects ; pathology ; Glutathione ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Sericins ; analysis ; pharmacology ; Superoxide Dismutase ; metabolism

OBJECTIVETo study the changes of mucosa irritation of crude and processed Radix Phytolaccae.

METHODGastrointestinal experiments on rats and mice and the rabbits' eyes irritation experiments were applied to investigate the changes of mucosa irritation of crude and processed Radix Phytolaccae.

RESULTThe mucosa irritation of processed Radix Phytolaccae decreased obviously compared to crude one.

CONCLUSIONAfter being processed with vinegar, the mucosa irritation on Radix Phytolaccae decreased obviously.

Acetic Acid ; chemistry ; Animals ; Dinoprostone ; metabolism ; Drug Compounding ; Drugs, Chinese Herbal ; adverse effects ; chemistry ; Eye ; drug effects ; Gastric Mucosa ; drug effects ; metabolism ; Male ; Mice ; Phytolacca ; chemistry ; Plant Roots ; chemistry ; Rats

The effects of thyroid hormone on hepatic and gastric alcohol dehydrogenase (ADH) activities (nM of NADH/min/mg of cytosolic protein) have been investigated in male Sprague Dawley rats treated with thyroxine (1 mg/kg, po) for 14 days. Whereas hepatic ADH activity in thyroxine-treated rats decreased by 61.3% of control rats (26.4 vs 43.2, p<0.001), gastric ADH activity increased by 262.9% of control rats (4.9 vs 1.9, p<0.001). As for the activities of the lung and kidney, thyroxine treatment did not produce any statistically significant changes. These data suggest that thyrotoxicosis causes a decrease of hepatic alcohol metabolism, and that the increase of gastric ADH activity in thyrotoxic rats can partly restore the first-pass metabolism of ethanol.
Alcohol Dehydrogenase/*metabolism ; Animal ; Gastric Mucosa/enzymology ; Kidney/enzymology ; Liver/drug effects/*enzymology ; Lung/enzymology ; Male ; Rats ; Rats, Sprague-Dawley ; Stomach/drug effects/*enzymology ; Thyrotoxicosis/chemically induced/metabolism ; Thyroxine/administration & dosage/*metabolism/pharmacology

OBJECTIVETo study the effects of Xinwei Granule (XG) on signal transducers and activators of transcription (STATs) and tyrosine phosphorylation of signal transducers and activators of transcription 3 (p-STAT3) signal pathway in rats with precancerous lesions of gastric carcinoma (PLGC).

METHODSTotally 96 Wistar rats were randomly divided into the blank control group (abbreviated as the blank group, n = 16) and the model group (n = 80). The PLGC rat model was established by complex pathogenic factors, in which methyl-N'-nitro-N-nitrosoguanidine (MNNG) was mainly used. After successful modeling, 75 rats randomly selected were divided into the model group, the Vitacoenzyme group, the low dose XG group, the middle dose XG group, and the high dose XG group, 15 in each group. Fifteen rats were randomly selected from the blank group, and fed with ordinary standard forage and administered with 10 mL/kg 0.9% sodium chloride by gastrogavage. XG at 1.254 g/kg, 2.508 g/kg, and 5.016 g/kg was respectively administered to rats in the three XG groups by gastrogavage. Rats in the model group were administered with 10 mL/kg 0.9% sodium chloride by gastrogavage. Vitacoenzyme was administered to rats in the Vitacoenzyme group. Vitacoenzyme Tablet was pulverized to prepare 0.1 g/mL 0.9% sodium chloride suspension and administered by gastrogavage. All the medication was performed once daily and continued for 12 weeks. The general conditions (including rats' fur, activity, food and water, excrement, body weight, and survival), the pathological changes in the gastric mucosa, as well as the expressions of STAT3 and p-STAT3 were observed.

RESULTSCompared with the blank group,the expression levels of STAT3 and p-STAT3 increased in the model group (P < 0.05). The general conditions, such as the activity, food and water intake, and body weight were improved in each XG group. Compared with the model group, the expressions of STAT3 and p-STAT3 decreased in each XG group with statistical difference (P < 0.05). The occurrence of PLGC, i.e., intestinal metaplasia (IM) and dysplasia (DYS) significantly decreased with statistical difference (P < 0.05). Compared with the Vitacoenzyme group, the occurrence of IM and DYS significantly decreased in the middle and high dose XG groups, showing statistical difference (P < 0.05). The expressions of STAT3 and p-STAT3 decreased more significantly in the middle and high dose XG groups, showing statistical difference (P < 0.05).

CONCLUSIONSXG could obviously improve the pathological conditions of gastric mucosa in rats with PLGC. It could fight against the progress of PLGC by down-regulating the expressions of STAT3 mRNA and p-STAT3.

Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Gastric Mucosa ; drug effects ; pathology ; Male ; Precancerous Conditions ; metabolism ; pathology ; Rats ; Rats, Wistar ; STAT3 Transcription Factor ; metabolism ; Signal Transduction ; drug effects ; Stomach Neoplasms ; metabolism ; pathology

BACKGROUND/AIMS: The prevalence of peptic ulcer disease has not decreased mainly due to an increase in the use of NSAIDs. This study was conducted in order to determine whether a chronic NSAID-induced gastric inflammation model could be established by repeated administration of NSAID. METHODS: Indomethacin (10 mg/kg) was administered once per week for six weeks in 8- and 26-week rats and animals were sacrificed every week after administration. Gross ulcer index, histologic damage index, myeloperoxidase (MPO) activity, and mucus (glucosamine) levels were measured. Small bowel damage was also evaluated. RESULTS: Gross gastric damage index showed a peak level at three weeks and then decreased slowly in the 26-week indomethacin group. Gastric mucosal glucosamine level increased in both the 8-week (p=0.038) and 26-week groups (p=0.007). In addition, gastric mucosal MPO level decreased in the 8-week group (p=0.018) but did not show a decrease in the 26-week group. Small bowel damage began to occur at three weeks during the schedule and eight of 36 rats (22.2%) died due to perforation or peritonitis of the small bowel in the 8- and 26-week indomethacin groups, respectively. CONCLUSIONS: Due to gastric adaptation and small bowel damage, repeated administration of NSAID to experimental animals may not be an adequate method for establishment of the chronic gastric inflammation model.
Animals ; Anti-Inflammatory Agents, Non-Steroidal/*toxicity ; Disease Models, Animal ; Gastric Mucosa/*drug effects/enzymology/pathology ; Glucosamine/metabolism ; Indomethacin/*toxicity ; Intestine, Small/*drug effects/pathology ; Male ; Peroxidase/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors