Effect of sofalcone on acute gastric mucosal lesions induced by aspirin and ethanol in reference to the biosynthesis of gastric mucosal glycoprotein.
Sofalcone prevented the formation of lesions by 50% ethanol and aspirin dose dependently, prevented the decrease in the gastric mucosal macromolecular glycoprotein content caused by these treatments, and prevented the decrease in the incorporation of 3H-glucosamine caused by ethanol and aspirin into the macromolecular glycoprotein. 35S-Sulfate incorporation, which was slightly decreased, by the administration of ethanol and aspirin, was significantly increased, and the specific activity of sulfated macromolecular glycoprotein synthesis which was not changed by ethanol or aspirin was increased by the administration of sofalcone prior to these treatments. These results suggest that the maintenance of the mucosal macromolecular glycoprotein content is involved in the protective effects of sofalcone against the formation of acute gastric lesions induced by ethanol and aspirin.
D000818:Animals; D001241:Aspirin / Q000037:antagonists & inhibitors*; D002599:Chalcone / Q000031:analogs & derivatives / Q000494:pharmacology*; D047188:Chalcones; D000431:Ethanol / Q000037:antagonists & inhibitors*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D005756:Gastritis / Q000139:chemically induced* / Q000503:physiopathology; D005944:Glucosamine / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism*; D008297:Male; D011427:Propiophenones / Q000494:pharmacology*; D051381:Rats; D013431:Sulfates / Q000378:metabolism; D014148:Tranexamic Acid / Q000031:analogs & derivatives / Q000494:pharmacology
D047188:Chalcones; D006023:Glycoproteins; D011427:Propiophenones; D013431:Sulfates; C035032:sofalcone; D000431:Ethanol; D002599:Chalcone; C000665:cetraxate; D014148:Tranexamic Acid; D005944:Glucosamine; D001241:Aspirin