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Inhibition of neutrophil activation by lafutidine, an H2-receptor antagonist, through enhancement of sensory neuron activation contributes to the reduction of stress-induced gastric mucosal injury in rats.
Dig Dis Sci. 2007 Feb; 52(2):469-77.DD

Abstract

Sensory neuron activation reduces water-immersion restraint stress (WIR)-induced gastric mucosal injury by inhibiting neutrophil activation through increase in endothelial production of prostacyclin. This study was designed to examine whether lafutidine, which is an H(2)-receptor antagonist and activates sensory neurons, inhibits neutrophil activation, thereby reducing WIR-induced gastric mucosal injury. Lafutidine enhanced WIR-induced increases in gastric tissue levels of calcitonin gene-related peptide (CGRP) and 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, whereas famotidine, another H(2)-receptor antagonist, did not. Such lafutidine-induced increases in gastric tissue levels of 6-keto-PGF(1alpha) were reversed by pretreatment with capsazepine, an inhibitor of sensory neuron activation, CGRP(8-37), a CGRP antagonist, and indomethacin. Lafutidine inhibited acid-induced exacerbation of gastric mucosal injury in animals subjected to WIR by inhibiting neutrophil activation, whereas famotidine did not. Lafutidine synergistically increased CGRP release from isolated rat dorsal root ganglion neurons in the presence of anandamide, but famotidine did not. These observations suggest that lafutidine might reduce WIR-induced gastric mucosal injury not only by inhibiting acid secretion but also by inhibiting neutrophil activation through enhancement of sensory neuron activation.

Authors+Show Affiliations

Department of Biodefense Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17211693

Citation

Harada, Naoaki, and Kenji Okajima. "Inhibition of Neutrophil Activation By Lafutidine, an H2-receptor Antagonist, Through Enhancement of Sensory Neuron Activation Contributes to the Reduction of Stress-induced Gastric Mucosal Injury in Rats." Digestive Diseases and Sciences, vol. 52, no. 2, 2007, pp. 469-77.
Harada N, Okajima K. Inhibition of neutrophil activation by lafutidine, an H2-receptor antagonist, through enhancement of sensory neuron activation contributes to the reduction of stress-induced gastric mucosal injury in rats. Dig Dis Sci. 2007;52(2):469-77.
Harada, N., & Okajima, K. (2007). Inhibition of neutrophil activation by lafutidine, an H2-receptor antagonist, through enhancement of sensory neuron activation contributes to the reduction of stress-induced gastric mucosal injury in rats. Digestive Diseases and Sciences, 52(2), 469-77.
Harada N, Okajima K. Inhibition of Neutrophil Activation By Lafutidine, an H2-receptor Antagonist, Through Enhancement of Sensory Neuron Activation Contributes to the Reduction of Stress-induced Gastric Mucosal Injury in Rats. Dig Dis Sci. 2007;52(2):469-77. PubMed PMID: 17211693.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of neutrophil activation by lafutidine, an H2-receptor antagonist, through enhancement of sensory neuron activation contributes to the reduction of stress-induced gastric mucosal injury in rats. AU - Harada,Naoaki, AU - Okajima,Kenji, Y1 - 2007/01/09/ PY - 2006/07/14/received PY - 2006/09/14/accepted PY - 2007/1/11/pubmed PY - 2007/4/4/medline PY - 2007/1/11/entrez SP - 469 EP - 77 JF - Digestive diseases and sciences JO - Dig Dis Sci VL - 52 IS - 2 N2 - Sensory neuron activation reduces water-immersion restraint stress (WIR)-induced gastric mucosal injury by inhibiting neutrophil activation through increase in endothelial production of prostacyclin. This study was designed to examine whether lafutidine, which is an H(2)-receptor antagonist and activates sensory neurons, inhibits neutrophil activation, thereby reducing WIR-induced gastric mucosal injury. Lafutidine enhanced WIR-induced increases in gastric tissue levels of calcitonin gene-related peptide (CGRP) and 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, whereas famotidine, another H(2)-receptor antagonist, did not. Such lafutidine-induced increases in gastric tissue levels of 6-keto-PGF(1alpha) were reversed by pretreatment with capsazepine, an inhibitor of sensory neuron activation, CGRP(8-37), a CGRP antagonist, and indomethacin. Lafutidine inhibited acid-induced exacerbation of gastric mucosal injury in animals subjected to WIR by inhibiting neutrophil activation, whereas famotidine did not. Lafutidine synergistically increased CGRP release from isolated rat dorsal root ganglion neurons in the presence of anandamide, but famotidine did not. These observations suggest that lafutidine might reduce WIR-induced gastric mucosal injury not only by inhibiting acid secretion but also by inhibiting neutrophil activation through enhancement of sensory neuron activation. SN - 0163-2116 UR - https://www.unboundmedicine.com/medline/citation/17211693/Inhibition_of_neutrophil_activation_by_lafutidine_an_H2_receptor_antagonist_through_enhancement_of_sensory_neuron_activation_contributes_to_the_reduction_of_stress_induced_gastric_mucosal_injury_in_rats_ DB - PRIME DP - Unbound Medicine ER -