Comparative Analysis of Gastroesophageal Reflux Disease Animal Model Methods: A Data Mining of the Past Decade.

Dig Dis Sci

Xiyuan Hospital, China Academy of Traditional Chinese Medicine, No. 1 Xiyuan Playground, Haidian District, Beijing, 100091, China.

Published: July 2025


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Article Abstract

Purpose: The differences in the animal model construction of different subtypes of gastroesophageal reflux disease (GERD) have not been clearly demonstrated at present. We aim to reveal the characteristics and differences between them.

Methods: The literature related to GERD animal model construction in the past decade was searched and data on animal strains, modeling modes, modeling cycles, and detection indices were extracted, and the results were presented by using descriptive statistical methods of frequency and relative frequency.

Results: 88 papers finally met the criteria. Sprague-Dawley (68.25%) rats were most often used to induce reflux esophagitis (RE), whereas Swiss mice (50.00%) and C57BL/6 mice (57.89%) for non-erosive reflux disease (NERD) and Barrett's esophagus (BE), respectively. RE and NERD were most frequently constructed using fore-stomach-glandular transition ligation together with pyloric insufficiency (37.68%, 50.00%), yet their median modeling cycles were 14 and 7 days, respectively. BE was most frequently constructed using L2-IL-1β transgenic mice (27.27%), and the median modeling cycle over 270 days. Determining esophageal mucosal permeability was common in NERD, while finding intestinal chemotaxis markers, squamous epithelium, and columnar epithelium was common in BE. In animal models of RE, researchers tended to look for markers associated with the inflammatory response and oxidative stress.

Conclusions: The induction methods vary among the animal models of GERD's three subtypes. Inflammatory stimulation is crucial for inducing RE and BE, differing in modeling cycle. In contrast, Visceral hypersensitivity draws more attention in NERD animal models, reflecting researchers' thoughts on distinct pathogenesis.

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http://dx.doi.org/10.1007/s10620-025-09022-xDOI Listing

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