[The protective effect of IL-1 beta on stress-induced gastric mucosal damage in rat].
The effect of recombinant IL-1 beta on stress-induced gastric mucosal lessions was studied in rats. Pretreatment with IL-1 beta prevented formation of gastric mucosal damage in a dose-dependent manner. IL-1 receptor antagonist peptide (IRAP) could totally reverse the protective effect of IL-1 beta. IL-1 fragment peptide (163-171) had no effect on gastric ulcer formation in the experimental model, whereas sulfhydryl blocker N-ehtylmaleimide partially blocked the protective effect of IL-1 beta. The concentration of protein and noneprotein sulfhydryls in the gastric mucosa was significantly decreased 3 h after stress, and this decrease was partially prevented by IL-1 beta. IL-1 beta also decreased the concentration of molondialdehyde (MDA) in the gastric mucosa after 3 h stress. The results suggest that IL-1 beta could effectively lessen the degree of stress-induced gastric mucosal damage, due possibly to the production of endogenous sulfhydryl compounds in the gastric mucosa.
D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000473:pathology; D007375:Interleukin-1 / Q000494:pharmacology*; D053583:Interleukin-1beta; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000494:pharmacology; D013276:Stomach Ulcer / Q000209:etiology / Q000517:prevention & control*; D013312:Stress, Physiological; D013438:Sulfhydryl Compounds / Q000378:metabolism
D000897:Anti-Ulcer Agents; D007375:Interleukin-1; D053583:Interleukin-1beta; D010446:Peptide Fragments; D011994:Recombinant Proteins; D013438:Sulfhydryl Compounds; C052994:interleukin-1beta (163-171)