BACKGROUND/AIMS: Low-dose aspirin therapy is widely used to prevent cardiovascular thrombotic events. However, the safety of low-dose aspirin therapy in the gastrointestinal tract is uncertain. Our aim was to evaluate endoscopic findings in patients taking low-dose aspirin. METHODS: Sixty-two patients who received 100 mg enteric coated aspirin daily more than 30 days were included in this study. Patients' medical records and endoscopic data were reviewed retrospectively. As controls, 70 of age- and gender-matched patients who received an endoscopy without gastrointestinal symptoms were employed. RESULTS: The overall prevalence of gastroduodenal mucosal injury was higher in the aspirin group than in the control group. Erosive gastritis was noted more frequently in the aspirin group than in the control group. However, the prevalence of ulcer was not different between the aspirin group and the control group. CONCLUSIONS: Patients treated with low-dose aspirin therapy are more likely to have endoscopic evidence of mucosal damage. Our study suggests that even a low-dose aspirin therapy can induce a gastroduodenal mucosal injury. In the future, a prospective randomized control study is needed.
Aged ; Aspirin/administration & dosage/*adverse effects ; Cardiovascular Diseases/prevention & control ; Esophagitis/chemically induced ; Female ; Gastritis/chemically induced ; Gastrointestinal Diseases/*chemically induced ; Humans ; Male ; Middle Aged ; Platelet Aggregation Inhibitors/administration & dosage/*adverse effects ; Tablets, Enteric-Coated/adverse effects

OBJECTIVETo explore the mechanisms of muscovite gastric mucosal protective effect.

METHODRat model of chronic gastritis were used. After gastric mucosal injury was induced, the rats were divided into 6 groups and were treated with different drugs. 2 weeks later, the tissue and blood samples were obtained and measured.

RESULTThe general conditions, the observations under macroscopy, microscope and electron microscope of the middle and high dose of muscovite groups resembled those of the normal group. Their PH levels were higher than those of the model group, and the rates of intestinal metaplasia were lower, but the PGE2 level of the middle dose of muscovite group was the highest.

CONCLUSIONMuscovite can be adsorbed on the surface of the gastric mucosa. It has gastric mucosal protective effect by improving excretion of mucus and synthesis of PGE2 in gastric mucosa, restraining gastric acid, reversing of intestinal metaplasia and decreasing inflammation cells.

Aluminum Compounds ; pharmacology ; Animals ; Dinoprostone ; blood ; Gastric Juice ; chemistry ; Gastric Mucosa ; pathology ; ultrastructure ; Gastritis ; blood ; chemically induced ; pathology ; Hydrogen-Ion Concentration ; Materia Medica ; pharmacology ; Microscopy, Electron, Scanning ; Potassium Compounds ; pharmacology ; Protective Agents ; pharmacology ; Rats ; Rats, Wistar ; Silicates ; pharmacology ; Sodium Salicylate

OBJECTIVETo study the effects and its possible mechanisms of total alkaloids (TA) from rhizoma Coptis chinensis on H. pylori LPS induced gastric lesion in rats.

METHODH. pylori lipopolysaccharide was applied to rat intragastrically for 4 days to induce a pattern of mucosal responses resembling that of acute gastritis. After treatment with 50, 100, 200 mg x kg(-1) TA, we identified the changes on gastric histopathology, the effects on the activities of cNOS and NOS-2, the contents of TNF-alpha and the gastric mucus epithelial cell apoptosis.

RESULTH. pylori LPS could significantly induce the epithelial cell apoptosis of gastric mucus, increase the expression of NOS-2 and decline the expression of cNOS, and enhance the content of TNF-alpha in serum. Treatment with 50, 100, 200 mg x kg(-1) TA led to reduction in the extent of mucosal inflammatory changes elicited by H. pylori LPS and decrease in epithelial cell apoptosis. Furthermore, this effect of TA was associated with decrease in content of TNF-alpha in serum, decline in NOS-2, and increase in cNOS.

CONCLUSIONThe findings suggest that TA is a potent protective agent against H. pylori LPS induced gastric mucosal inflammation. The concerned mechanisms may be related to its inhibition on epithelial cell apoptosis, and the suppression of the inflammatory responses by upregulating cNOS and interfering with the events propagated by NOS-2, and reducing the content of TNF-alpha.

Acute Disease ; Alkaloids ; isolation & purification ; pharmacology ; Animals ; Apoptosis ; drug effects ; Coptis ; chemistry ; Epithelial Cells ; drug effects ; enzymology ; pathology ; Gastric Mucosa ; drug effects ; enzymology ; pathology ; Gastritis ; blood ; chemically induced ; prevention & control ; Lipopolysaccharides ; Male ; Nitric Oxide Synthase Type II ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Plants, Medicinal ; chemistry ; Protective Agents ; isolation & purification ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Rhizome ; chemistry ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo investigate the mechanism of isinglass in the prevention and treatment of chronic atrophic gastritis (CAG) in rats.

METHODAnimal models of SD rats with CAG were made in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while CAG rat model was being made. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed. Then the length of the proliferation zone of the gastric mucosa and serum epidermal growth factors (EGF) and growth hormones (GH)level were studied.

RESULTIn isinglass prevention groups and high dose isinglass reverse group, the length of the proliferation zone of the gastric mucosa was very close to that in normal control group (P > 0.05), much better than model control group (P < 0.01). In low dose isinglass reverse group, it was lower than that in normal control group (P < 0.01), but much better than model control group (P < 0.01). In both prevention and reverse groups, serum EGF level was higher than that in normal (P < 0.01) and model control group (P < 0.05). Serum GH level was the same in every group (P > 0.05).

CONCLUSIONThe mechanism of isinglass in the prevention and treatment of CAG rats lies in revitalizing and proliferating gastric mucosal cells by stimulating endogenous EGF secretion.

Animals ; Chronic Disease ; Dose-Response Relationship, Drug ; Epidermal Growth Factor ; blood ; Female ; Gastritis, Atrophic ; chemically induced ; drug therapy ; prevention & control ; Gelatin ; administration & dosage ; therapeutic use ; Growth Hormone ; blood ; Materia Medica ; administration & dosage ; therapeutic use ; Proliferating Cell Nuclear Antigen ; metabolism ; Rats ; Rats, Sprague-Dawley