ArticleNeurogastroenterology and motility2026
Impact of PAR2 on Tight Junctions and Esophageal Mucosal Inflammation in Rats with Gastroesophageal Reflux Disease.
Article in Neurogastroenterology and motility, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGastric content reflux activates protease-activated receptor 2 (PAR2), which is a critical step in the pathophysiological mechanisms underlying gastroesophageal reflux disease (GERD). Claudins serve as the primary constituents of tight junctions (TJs). They are in charge of the barrier and polarity of epithelial cells, and the disruption of their function can lead to chronic inflammation. The present research is designed to investigate whether PAR2 influences TJs in the development of GERD.
methodsGERD models were established both in vivo and in vitro. Rabeprazole and/or GB-88 (a PAR2 inhibitor) were administered. The expression of PAR2, Claudin-1, and Claudin-4, M1 macrophages, transepithelial electrical resistance (TEER), Interleukin-8 (IL-8), and Interleukin-1β (IL-1β) were measured. Furthermore, cells were treated with SLIGKV-NH2 (a PAR2 agonist) and GB-88 to verify the impact of PAR2 on TJs.
resultsRabeprazole improved pathological changes, decreased the concentration of IL-8 and IL-1β, and inhibited the accumulation of M1 macrophages in GERD rats. Rabeprazole inhibited the expression of PAR2 and enhanced Claudin-1 and Claudin-4 in vivo. GB-88 declined PAR2 and the concentration of IL-8 and IL-1β, and increased Claudin-1, Claudin-4, and TEER in vitro. The combination of GB-88 and rabeprazole was more effective in restoring Claudin-4.
conclusionIn GERD, elevated PAR2 expression impaired esophageal mucosal barrier function by downregulating and inducing the redistribution of Claudin-1 and Claudin-4, while promoting M1 macrophage-mediated secretion of IL-8 and IL-1β.
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