Study on the acceleration in healing of ethanol-induced gastric lesions in rats by methylprednisolone.

This study was designed to determine the influences of methylprednisolone (MP, CAS 2375-03-3) on the genesis and healing of gastric lesions induced by 50% ethanol in relation to the changes in gastric mucosal prostaglandin (PG) and leukotriene (LT) contents and vascular permeability. Intragastric administration of 1 ml of 50% ethanol induced hemorrhagic lesions in the fundic portion, and these lesions were not affected by 20 mg/kg of MP injected subcutaneously 30 min before ethanol administration. In untreated rats, 4 kinds of PGs, i.e., 6-keto-PGF1a, PGF2a, PGE2, and PGD2, were determined in gastric mucosa by high performance liquid chromatography (HPLC), but no LTs were detected. Administration of ethanol significantly reduced all PG contents and increased production of peptide-LTs in gastric mucosa. Pretreatment with MP did not influence ethanol-induced changes in PG and peptide-LT contents. Ethanol-induced lesions required 96 h for total healing. Ulcer healing was not affected by MP, which was injected subcutaneously twice daily from 1 h after ethanol administration until the end of the experiment, and complete ulcer healing was observed after 72 h. MP did not affect ethanol-induced decrease in PG contents, their recoveries, or peptide-LT contents. Ethanol increased vascular permeability and MP reduced this increase. These results suggest that MP does not have a hazardous effect, but is rather beneficial with regard to healing of ethanol-induced gastric lesions through prevention of the increase in vascular permeability caused by ethanol, and that it affected neither gastric mucosal PG nor peptide-LT contents.