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碘乙酰胺诱导大鼠胃炎后胃黏膜中 TRPA1 离子通道的上调：一个潜在的新治疗靶点。

Upregulation of the TRPA1 Ion Channel in the Gastric Mucosa after Iodoacetamide-Induced Gastritis in Rats: A Potential New Therapeutic Target.

机构信息

Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, H-7624 Pécs, Hungary.

Szentagothai Research Centre, University of Pécs, H-7624 Pécs, Hungary.

出版信息

Int J Mol Sci. 2020 Aug 5;21(16):5591. doi: 10.3390/ijms21165591.

DOI:10.3390/ijms21165591
PMID:32764237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7460663/
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. 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 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.

摘要

急性胃炎通常不能通过抑制胃酸分泌的药物治疗。了解包括瞬时受体电位锚蛋白 1（TRPA1）和香草素 1（TRPV1）通道在内的保护机制，这些通道位于辣椒素敏感传入神经和非神经元结构上，可能确定新的治疗方法。因此，我们使用碘乙酰胺（IAA）描述了一种转化性胃炎模型，并研究了 TRPA1/V1 的表达。Wistar 大鼠和 CD1、C57Bl/6J 小鼠暴露于含有 IAA（0.05、0.1、0.2、0.3、0.5%）的饮用水中 7 或 14 天。每天记录体重和饮水量。对宏观病变进行评分，进行定性组织病理学检查，测量 TRPA1/V1 免疫阳性和 mRNA 表达。IAA 在两种物种中均诱导浓度依赖性的体重减轻和水摄入量减少。7 天后，大鼠出现充血、黏膜下水肿、炎症浸润和出血性糜烂，而 14 天后则出现溃疡。在两个时间点，mRNA/蛋白表达均上调。同时，在摄入 0.05% IAA 后，胃体中的 TRPV1 免疫阳性上调，但在摄入 0.2% 后下调，而 mRNA 没有变化。有趣的是，在小鼠中没有观察到宏观/微观变化。这些是大鼠中 IAA 诱导的胃炎浓度和时间依赖性变化的首批数据，伴随 TRPA1 上调，因此应进一步研究其在胃炎中的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/712d/7460663/c0060c90b602/ijms-21-05591-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/712d/7460663/789e395c7fb1/ijms-21-05591-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/712d/7460663/680ca403157b/ijms-21-05591-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/712d/7460663/806612f16a47/ijms-21-05591-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/712d/7460663/580903d273e4/ijms-21-05591-g008.jpg
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