Abstract
Acute gastritis is often untreatable by acid secretion-inhibiting drugs. Understanding the protective mechanisms including the role of Transient Receptor Potential Ankyrin1 (TRPA1) and Vanilloid1 (TRPV1) channels localized on capsaicin-sensitive afferents and non-neuronal structures might identify novel therapeutic approaches. Therefore, we characterized a translational gastritis model using iodoacetamide (IAA) and investigated TRPA1/V1 expressions. Wistar rats and CD1, C57Bl/6J mice were exposed to IAA-containing (0.05, 0.1, 0.2, 0.3, 0.5%) drinking water for 7 or 14 days. Body weight and water consumption were recorded daily. Macroscopic lesions were scored, qualitative histopathologic investigation was performed, TRPA1/V1 immunopositivity and mRNA expressions were measured. IAA induced a concentration-dependent weight loss and reduced water intake in both species. Hyperemia, submucosal edema, inflammatory infiltration and hemorrhagic erosions developed after 7 days, while ulcers after 14 days in rats. Trpa1 mRNA/protein expressions were upregulated at both timepoints. Meanwhile, TRPV1 immunopositivity was upregulated in the gastric corpus after 0.05% IAA ingestion, but downregulated after 0.2%, whereas Trpv1 mRNA did not change. Interestingly, no macroscopic/microscopic changes were observed in mice. These are the first data for the concentration- and duration-dependent changes in the IAA-induced gastritis in rats accompanied by TRPA1 upregulation, therefore, its therapeutic potential in gastritis should further be investigated.
Highlights
Gastric mucosal injury can be exhibited by various forms of macroscopic and histopathological alterations, such as diffuse hyperemia, inflammation, erosion, or even hemorrhagic ulcerations
Macroscopic and Microscopic Picture negative negative negative negative negative negative. This is the first comprehensive and comparative acute and chronic diffuse gastritis model study, in which IAA-induced concentration- and duration-dependent changes were described in Wistar rats
IAA induced concentration-dependent weight loss and gastric erosions already after 7-day ingestion of IAA in drinking water accompanied by massive submucosal edema and extensive infiltration by acute and chronic inflammatory cells, and subsequently, hemorrhagic erosions
Summary
Gastric mucosal injury can be exhibited by various forms of macroscopic and histopathological alterations, such as diffuse hyperemia, inflammation, erosion, or even hemorrhagic ulcerations. IAA treatment increased tGSH (based on the peak area in mAU of the GSH peak) numerically, but not significantly in the rat gastric mucosa: 2.55 ± 0.85 in the control group; 3.15 ± 1.21 in the group treated with 0.1% IAA for 7 days; and 3.25 ± 0.82 in the group treated with 0.1% IAA for 14 days (Figure 5B). Socil.a2r02ra0,ti2o1,, 5w59h1ich was not significant: 2.43 ± 0.72; 2.13 ± 0.77; 1.98 ± 0.39, respectively (data n7 ootf 18 shown)
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