Abstract
In this study, a rat model with acetic acid-induced PI-IBS was used to study the role of HXZQ oral liquid in repairing the colonic epithelial barrier and reducing intestinal permeability. Pathomorphism of colonic tissue, epithelial ultrastructure, DAO activity in serum, and the protein expression of ZO-1 and occludin were examined to investigate protective effect mechanisms of HXZQ on intestinal mucosa barrier and then present experimental support for its use for prevention and cure of PI-IBS.
Highlights
Postinfectious irritable bowel syndrome (PI-IBS) is a common disorder wherein symptoms of IBS begin after an episode of acute gastroenteritis
The components obtained from using an infinity high-performance liquid chromatography (UPLC) analysis of HXZQ oral liquid and standard mixtures were detected at 220 nm
Our results suggest that alteration of tight junction proteins may be involved in the initiation of PI-IBS and HXZQ can upregulate the expression of ZO-1 and occludin protein, which suggests that the tight junction afforded by occludin and ZO-1 is important in maintaining the epithelial barrier integrity in response to HXZQ
Summary
Postinfectious irritable bowel syndrome (PI-IBS) is a common disorder wherein symptoms of IBS begin after an episode of acute gastroenteritis. Recent studies have suggested that increased intestinal permeability could be an important factor in the sequence of events leading to low-grade intestinal inflammation and disturbed bowel function [8, 9]. Intestinal epithelial permeability is regulated by a complex protein system comprising tight junction (TJ) and adherens junction proteins [10]. This increased permeability could be due to alterations of tight junction proteins. There are no successful treatments for PI-IBS, and management of PI-IBS primarily aims at relieving the symptoms [12, 13]
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