Abstract

Intestinal barrier dysfunction occurs in many intestinal diseases, in which proinflammatory cytokines play critical roles. However, researchers are still on the way to defining the underlying mechanisms and to evaluate therapeutic strategies for restoring intestinal barrier function. Berberine, a drug that has clinically been used to treat gastroenteritis and diarrhea for thousands of years, has been shown to protect barrier function in both endothelial and epithelial cells, but the mechanisms are completely unknown. In this study, we investigate the protective actions of berberine on barrier function and the underlying mechanisms in Caco-2 monolayers challenged with IFN-γ and TNF-α. Caco-2 monolayers were treated without or with simultaneous IFN-γ and TNF-α in the absence or presence of berberine. Both transepithelial electrical resistance (TER) and paracellular permeability were measured to evaluate barrier function. The expression and distribution of tight junction proteins ZO-1, occluding, and claudin-1 were respectively analyzed by immunoblot or immunofluorescence. The expressions of phosphorylated myosin light chain (pMLC), MLC kinase (MLCK) and hypoxia-inducible factor-1α (HIF-1α) were determined by immunoblot. The translocation of NF-κB p65 to nuclei was analyzed by immunofluorescence and immunoblot, respectively. The results showed that berberine significantly attenuated TER decrease and paracellular permeability increase in Caco-2 monolayers treated with IFN-γ and TNF-α. Berberine also dramatically alleviated IFN-γ and TNF-α-induced morphological alteration of tight junction proteins ZO-1, occluding, and claudin-1. The increase of both MLC phosphorylation and MLCK protein expression induced by IFN-γ and TNF-α was significantly inhibited by berberine treatment. Additionally, berberine suppressed the activation of HIF-1α, but not NF-κB. Taken together, it is suggested that berberine attenuates IFN-γ and TNF-α-induced intestinal epithelial barrier dysfunction by inhibiting the signaling pathway of MLCK-dependent MLC phosphorylation mediated by HIF-1α.

Highlights

  • It is well known that an intact intestinal epithelial barrier plays an important role in preventing luminal pathogens and antigenic molecules from coming into the intestinal mucosa and contacting with the immune system, and that tight junction and its associated proteins, such as zonula occludens (ZO), occludin and claudins, are critical to the maintenance of the intact intestinal epithelial barrier [1,2,3,4]

  • The underlying mechanisms are incompletely understood, it has been believed that myosin light chain (MLC) phosphorylation mediated by MLC kinase (MLCK) plays a very important role in the proinflammatory cytokinesinduced intestinal barrier disruption [9,10,11,13,15]

  • In order to investigate the effect of berberine on intestinal barrier function, we adopted an in vitro model in which human colonic Caco-2 epithelial cell monolayers were treated with simultaneous IFN-c and tumor necrosis factor (TNF)-a for 48 hours [33,34]

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Summary

Introduction

It is well known that an intact intestinal epithelial barrier plays an important role in preventing luminal pathogens and antigenic molecules from coming into the intestinal mucosa and contacting with the immune system, and that tight junction and its associated proteins, such as zonula occludens (ZO), occludin and claudins, are critical to the maintenance of the intact intestinal epithelial barrier [1,2,3,4]. During the process of these enteropathies, many proinflammatory cytokines are released within the intestinal mucosa These proinflammatory cytokines including interferon (IFN)-c, tumor necrosis factor (TNF)-a, interleukin (IL)1b, IL-6, IL-13 and TNF superfamily member LIGHT have been documented to contribute to the disruption of intestinal epithelial barrier function [4,8,9,10,11,12,13,14,15]. The compromised disruption of intestinal barrier function may be either causative or consequential, it has been proposed to play a very important role in the pathogenesis and relapse of inflammatory bowel disease including Crohn’s disease and ulcerative colitis [16,17,18]. Restoring the disrupted intestinal barrier function is beneficial for eliminating or alleviating the mucosal inflammation and immune responses

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