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通过过量进食诱导小鼠发生胃食管反流病的非手术动物模型。

Non-surgical animal model of gastroesophageal reflux disease by overeating induced in mice.

机构信息

Department of Otorhinolaryngology-Head and Neck Surgery, Korea University Medicine, Seoul, South Korea.

Neuroscience Research Institute, Korea University Medicine, Seoul, South Korea.

出版信息

J Investig Med. 2021 Aug;69(6):1208-1214. doi: 10.1136/jim-2020-001691. Epub 2021 Apr 16.

Abstract

Previous animal models of gastroesophageal reflux disease (GERD) were not physiological and required a variety of surgical procedures. Therefore, the animal model developed by conditions that are similar to the pathogenesis of GERD is necessary. The aim is to establish a non-surgical animal model with GERD caused by overeating induced in mice. To induce mice to overeat, we designed dietary control protocols including repetitive fasting and feeding. The esophageal tissues were evaluated with GERD markers to prove the establishment of a GERD animal model. Mice fasted every other day (group 2) showed more pronounced overeating feature and demonstrated evident changes similar to the macroscopic and microscopic findings of GERD, the expressions of inducible nitric oxide synthase and substance P were stronger. The higher frequency of fasting and overeating could cause GERD effectively. The dietary control can make mice overeat, which elicits the change of lower esophageal mucosa similar to GERD. Thus, the overeating-induced mouse may be used as a GERD mouse model.

摘要

先前的胃食管反流病(GERD)动物模型并不符合生理条件,且需要进行多种外科手术。因此,有必要开发一种与 GERD 发病机制相似的动物模型。本研究旨在建立一种由过量饮食诱导的非手术性小鼠 GERD 动物模型。为了诱导小鼠过量进食,我们设计了包括重复禁食和喂养的饮食控制方案。使用 GERD 标志物评估食管组织,以证明 GERD 动物模型的建立。隔天禁食的小鼠(第 2 组)表现出更明显的暴食特征,并表现出与 GERD 的宏观和微观发现相似的明显变化,诱导型一氧化氮合酶和 P 物质的表达更强。禁食和暴食的频率越高,越能有效地引起 GERD。饮食控制可使小鼠暴食,引起食管下黏膜的变化类似于 GERD。因此,诱导性暴食的小鼠可作为 GERD 小鼠模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/568b/8327402/b467d65e0bf6/jim-2020-001691f01.jpg

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