Activated neutrophils impair gastric cytoprotection role of neutrophil elastase
Research article published in Digestive diseases and sciences (2000)
Abstract
Neutrophil elastase decreases production of PGI2 by cultured endothelial cells. Thus, neutrophil elastase may play an important role in gastric mucosal injury by decreasing the tissue level of PGI2, an important gastric cytoprotective substance. We examined whether activated neutrophils inhibit gastric PGI2 production in rats subjected to water-immersion restraint stress. Gastric 6-keto-PGF1alpha levels were determined by enzyme immunoassay. Gastric mucosal blood flow was determined by laser-Doppler flowmeter. Gastric microvascular permeability was determined by Evans blue leakage. Gastric levels of 6-keto-PGF1alpha were transiently increased 0.5 hr after the stress, followed by a decrease to below baseline at 6 hr, when mucosal blood flow fell to 60% of baseline. Gastric levels of 6-keto-PGF1alpha were significantly higher in animals with nitrogen mustard-induced leukocytopenia than in controls 1 and 6 hr after the stress. In leukocytopenic animals, levels 6 hr after stress were not lower than those preceding stress. Leukocytopenia markedly limited both the decrease in mucosal blood flow and the increase in gastric microvascular permeability. The level of gastric mucosal injury observed 6 hr after the stress was markedly attenuated by leukocytopenia. Pretreatment with neutrophil elastase inhibitors (ONO-5046 and Eglin C) or an anti-P-selectin monoclonal antibody produced effects similar to leukocytopenia. Neutrophil elastase is involved in the stress-induced gastric mucosal injury by decreasing gastric production of PGI2. Thus, pharmacologic inhibition of neutrophil elastase should help to prevent stress-induced gastric mucosal injury.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Neutrophil elastase decreases production of PGI2 by cultured endothelial cells.
Por qué esto importa para la hirudoterapia
Este estudio en ratas examinó si los neutrófilos activados deterioran la citoprotección gástrica al disminuir la producción de PGI2 durante el estrés por inmovilización con inmersión en agua, hallando que la elastasa de neutrófilos contribuye a la lesión de la mucosa gástrica inducida por estrés al reducir los niveles gástricos de PGI2. El pretratamiento con inhibidores de la elastasa de neutrófilos (ONO-5046 y Eglin C) atenuó la lesión mucosa, disminuyó la permeabilidad microvascular y preservó el flujo sanguíneo. Si bien Eglin C es reconocido en la literatura científica más amplia como una proteína derivada de la sanguijuela, este resumen no menciona sanguijuelas, hirudoterapia ni el secretoma de la sanguijuela, por lo que no se establece ninguna conexión defendible con el ámbito de ASH a partir del resumen en solitario. El estudio es preclínico (modelo animal) y se centra en los mecanismos de lesión de la mucosa gástrica mediados por neutrófilos.
Citación
Activated neutrophils impair gastric cytoprotection role of neutrophil elastase
Harada N et al. · Digestive diseases and sciences, 2000
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026