Abstract

This study was carried out to investigate protective effect of chlorogenic acid against lipopolysaccharide-induced inflammation and oxidative stress in intestinal epithelial cells. As a marker of inflammatory response, IL-6, IL-8, TNF-α mRNA and protein levels, furthermore, COX-2 mRNA level were followed up. Intracellular redox status and extracellular H2O2 level were also monitored by two fluorescent assays (DCFH-DA, Amplex Red). Moreover, the effect of gut microbiota metabolites in the above mentioned processes was taken into account in our model using Lactobacillus plantarum 2142 bacterial strain. Our data revealed that chlorogenic acid had significant lowering effect on the inflammatory response. Treatment with chlorogenic acid (25–50 μM) significantly decreased gene expression and concentration of proinflammatory cytokines IL-6 and IL-8 compared to LPS-treated cells. COX-2 and TNF-α mRNA levels were also reduced. Furthermore, chlorogenic acid reduced the level of reactive oxygen species in IPEC-J2 cells. Simultaneous application of chlorogenic acid and Lactobacillus plantarum 2142 supernatant resulted protective effect against LPS-induced inflammation and oxidative stress as well.

Highlights

  • The gut has two important functions, i.e. the digestion and host defence

  • Thirty-three % of the IPEC-J2 cells were killed by 1 h treatment when chlorogenic acid was applied at 100 μM concentrations

  • When cells were treated for 4 h with chlorogenic acid using different concentrations, reduced viability was measured compared to the control samples

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Summary

Introduction

The gut has two important functions, i.e. the digestion and host defence. Impact of environmental stress and infections caused by pathogens could lead to dysfunctional epithelium; chronic inflammatory disorders (e.g. Crohn’s disease and ulcerative colitis) and other kind of diseases could be developed such as type 1 diabetes [1,2,3]. The fact that presence of chronic inflammation in the gastrointestinal system is correlated with increased cancer risk is widely known, because of sharing the same signal transduction pathways [4].

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