Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently it has been reported that Shosaiko-to (SHO), a traditional Chinese medicine used for treating gastritis and hepatitis, also has been found useful for treating gastric ulcers, although no pharmacological study has yet investigated the precise antiulcer properties of SHO. Herein, the authors report on the results of a rat study in which the effects of SHO on gastric ulcers, acid secretions and potential difference of gastric mucosa (PD) were studied. SHO (100, 250 or 500 mg /kg, p.o.) significantly inhibited the development of ethanol-induced gastric lesions in a dose-dependent manner. SHO (500 mg/kg, p.o.) significantly inhibited the development of aspirin-,indomethacin- or water-immersion-stress induced gastric lesions. Sucralfate (500 mg/kg, p.o.) inhibited both ethanol- and aspirin-induced gastric lesions, and cimetidine (10 mg/kg, p.o.) inhibited aspirin-, indomethacin- or stress-induced gastric lesions. SHO (10, 30 and 100 mg/kg, i.p.) also significantly inhibited pentagastrin- and 2-deoxy-D-glucose (2-DG)-induced gastric acid secretions in a dose-dependent manner, whereas cimetidine (1 mg/kg, i.p.) inhibited a pentagastrin-induced secretion and atropine (0.05 mg/kg, i.p.) inhibited pentagastrin- or 2-DG-induced acid secretions. SHO (250, 500 or 1000 mg/kg, i.g.) significantly inhibited ethanol-induced PD reduction. Sucralfate (500 mg/kg, i.g.) inhibited the reduction, and cimetidine (250 mg/kg, i.g.) didn't inhibit it. These results indicate that SHO not only possesses the capability of protecting the rat gastric mucosa as well as sucralfate, but also is able to inhibit gastric acid secretions like cimetidine or atropine.
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PMID:[Antiulcer properties of shosaiko-to]. 894 Jul 3

Patients with hepatic injury have an increased incidence of gastric ulcers and erosions. In this study, the effect of D-galactosamine(GalN)-induced hepatitis on ethanol-induced gastric mucosal lesions and the protective effect of anti-ulcer agents in rats were examined. Subcutaneous injection of GalN (1 g/kg) remarkably increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities suggesting induction of hepatic injury. Gastric mucosal lesions induced by ethanol were significantly aggravated in GalN-induced hepatitis rats. Orally administered ecabet (CAS 86408-72-2; 20-200 mg/kg) dose dependently inhibited ethanol-induced gastric mucosal lesions in GalN-induced hepatitis rats. Sucralfate (CAS 54182-58-0) tended to inhibit the gastric mucosal lesions at a dose of 200 mg/kg but teprenone (CAS 6809-52-5), cimetidine (CAS 51481-61-9) and rebamipide (CAS 90098-04-7) had little effect. All anti-ulcer agents had no effect on the serum ALT and AST activities increased by GalN pretreatment. These results indicate that the gastric mucosa of GalN-induced hepatitis rats is more susceptible to injury induced by luminal irritants such as ethanol. Ecabet potently inhibited gastric mucosal lesions suggesting its clinical utility for the gastric mucosal damage in patients with hepatic injury.
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PMID:Effects of anti-ulcer agents on ethanol-induced gastric mucosal lesions in D-galactosamine-induced hepatitis rats. 1223 47