Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.

Since recent studies suggest an imbalance between cathepsin B and its tissue protease inhibitors (PI) in the pathogenesis of acute and chronic diseases, we tested the hypothesis that release of activated cysteine proteases (P) such as cathepsins B, H, and L might play a role in the pathogenesis of g...

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Main Authors: Nagy, L, Kusstatscher, S, Hauschka, P V, Szabo, S
Formato: Artigo
Idioma:English
Publicado em: 1996
Assuntos:
Research Article
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC507521/
https://ncbi.nlm.nih.gov/pubmed/8770878
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spelling pubmed-5075212004-11-12 Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat. Nagy, L Kusstatscher, S Hauschka, P V Szabo, S J Clin Invest Research Article Since recent studies suggest an imbalance between cathepsin B and its tissue protease inhibitors (PI) in the pathogenesis of acute and chronic diseases, we tested the hypothesis that release of activated cysteine proteases (P) such as cathepsins B, H, and L might play a role in the pathogenesis of gastric hemorrhagic mucosal lesions (HML) induced by ethanol (E) or ammonia (A). Anesthetized rats received 1 ml of 50% E or 1% A solution intragastrically for 1 min during in situ gastric luminal perfusion. Rapid activation and release of cathepsins B, L, and H into the luminal perfusate preceded the formation of HML quantified by planimetry. Mucosal presence and activity of cysteine PI and cathepsin B have also been investigated in the pathogenesis of chemically induced HML. We extracted and partially isolated acid and thermostable inhibitors of cathepsin B in the gastric mucosa, and found rapid inactivation of PI and activation of cathepsin B in the early phase of E- or A-induced HML. Negative correlations were found between P and PI activities by E or A solutions. Both the activation of cathepsins B, L, and H and the development of E-induced HML were prevented by pretreatment with the sulfhydryl alkylator N-ethylmaleimide. These results suggest that cysteine P may be activated in the rat stomach after E or A exposure, and cysteine P may have a role in the pathogenesis of E- or A-induced gastric HML. Endogenous PI may also participate in the mechanisms of gastric mucosal lesions and gastroprotection. 1996-08-15 /pmc/articles/PMC507521/ /pubmed/8770878 Text en
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Research Article
spellingShingle Research Article
Nagy, L
Kusstatscher, S
Hauschka, P V
Szabo, S
Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
description Since recent studies suggest an imbalance between cathepsin B and its tissue protease inhibitors (PI) in the pathogenesis of acute and chronic diseases, we tested the hypothesis that release of activated cysteine proteases (P) such as cathepsins B, H, and L might play a role in the pathogenesis of gastric hemorrhagic mucosal lesions (HML) induced by ethanol (E) or ammonia (A). Anesthetized rats received 1 ml of 50% E or 1% A solution intragastrically for 1 min during in situ gastric luminal perfusion. Rapid activation and release of cathepsins B, L, and H into the luminal perfusate preceded the formation of HML quantified by planimetry. Mucosal presence and activity of cysteine PI and cathepsin B have also been investigated in the pathogenesis of chemically induced HML. We extracted and partially isolated acid and thermostable inhibitors of cathepsin B in the gastric mucosa, and found rapid inactivation of PI and activation of cathepsin B in the early phase of E- or A-induced HML. Negative correlations were found between P and PI activities by E or A solutions. Both the activation of cathepsins B, L, and H and the development of E-induced HML were prevented by pretreatment with the sulfhydryl alkylator N-ethylmaleimide. These results suggest that cysteine P may be activated in the rat stomach after E or A exposure, and cysteine P may have a role in the pathogenesis of E- or A-induced gastric HML. Endogenous PI may also participate in the mechanisms of gastric mucosal lesions and gastroprotection.
author Nagy, L
Kusstatscher, S
Hauschka, P V
Szabo, S
author_facet Nagy, L
Kusstatscher, S
Hauschka, P V
Szabo, S
author_sort Nagy, L
title Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
title_short Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
title_full Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
title_fullStr Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
title_full_unstemmed Role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
title_sort role of cysteine proteases and protease inhibitors in gastric mucosal damage induced by ethanol or ammonia in the rat.
publishDate 1996
url https://ncbi.nlm.nih.gov/pmc/articles/PMC507521/
https://ncbi.nlm.nih.gov/pubmed/8770878
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