Vitamin A prevents lipopolysaccharide-induced injury on tight junctions in mice.

Caimei He,Mei Peng,Jingtao Wu,Di Xiao,Xiaoping Yang,Simeng Xu,Xin Hu,Sichun Zhou,Yanjun Huang,Jun Deng

doi:10.1002/fsn3.1481

Abstract

Vitamin A (VA) is one of the most widely used food supplements, but its molecular mechanisms largely remain elusive. Previously, we have demonstrated that VA inhibits the action of lipopolysaccharide (LPS) on intestinal epithelial barrier function and tight junction proteins using IPEC‐J2 cells, one of representative intestinal cell lines as a cellular model. These exciting findings stimulated us continue to determine the effects of VA on LPS‐induced damage of intestinal integrity in mice. Our results demonstrated that LPS treatment caused reductions of the mRNA levels of tight junction proteins including Zo‐1, Occludin, and Claudin‐1, well‐known biomarkers of intestinal integrity, and these reductions were reversed by VA pretreatment. Intestinal immunofluorescent results of Claudin‐1 revealed that LPS disrupted the structure of tight junction and reduced the expression of Claudin‐1 at protein level, which was reversed by VA pretreatment. These results suggest that VA may exert a profound role on preventing intestinal inflammation in vivo.

Highlights

Vitamin A (VA) is a commonly used food supplement that maintains visual function, tissue development, differentiation, and immune response
The development of most diseases is related to the intestinal epithelial barrier in the clinic, and the intestine has a function of separating the substances in the intestinal lumen and preventing the invasion of pathogenic antigens (Buckley & Turner, 2018; De Santis, Cavalcanti, Mastronardi, Jirillo, & Chieppa, 2015)
For Claudin-1 staining, cryosection of intestine tissues was fixed with 2% (v/v) formaldehyde in PBS for 30 min and incubated with 1% (v/v) Triton X-100 in PBS 3 times for 5 min each to permeabilize cells and washed and blocked for 30 min with 1% (w/v) bovine serum albumin (BSA) in PBS

Summary

| INTRODUCTION

Vitamin A (VA) is a commonly used food supplement that maintains visual function, tissue development, differentiation, and immune response. VA plays an essential role in tight junctions in vitro (Osanai, 2017; Rybakovsky et al, 2017). Tight junctions are important components of the intestinal epithelial barrier. Alteration of tight junctions is becoming an important biomarker of determining the function of intestine (Wardill, Gibson, Logan, & Bowen, 2014). Studies have confirmed that LPS, one commonly and important inflammation activator, produces damages on tight junctions in vitro (Chen et al, 2015; Main, Weber, Baumgard, & Gabler, 2012). We have shown that VA protected against LPS-induced damage on tight junctions in vitro (He et al, 2019). Whether or how effect of VA on tight junction of intestine in vivo remains elusive. We use miniature mice to further explore the effect of VA on tight junctions in vivo

| MATERIALS AND METHODS

| DISCUSSION

| CONCLUSIONS