Eugenol attenuates inflammatory response and enhances barrier function during lipopolysaccharide (LPS)-induced inflammation in the porcine intestinal epithelial (IPEC-J2) cells

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Date
2020-08
Authors
Hui, Qianru
Ammeter, Emily
Liu, Shangxi
Yang, Runqiang
Lu, Peng
Lahaya, Ludovic
Yang, Chengbo
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Abstract
Eugenol (4-allyl-2-methoxyphenol) is an essential oil component, possessing anti-microbial, anti-inflammatory and anti-oxidative properties, however the effect of eugenol on porcine gut inflammation has not yet been investigated. In this study, an in vitro lipopolysaccharide (LPS)-induced inflammation model in porcine intestinal epithelial cells (IPEC-J2) has been set up. Cells were pre-treated with 100 μM (16.42 mg/L) eugenol for 2 h followed by 10 μg/mL LPS stimulation for 6 h. Pro-inflammatory cytokine secretion, reactive oxygen species, gene expression of pro-inflammatory cytokines, tight junction proteins and nutrient transporters, the expression and distribution of zonula occludens-1 (ZO-1), trans-epithelial electrical resistance (TEER) and cell permeability were measured to investigate the effect of eugenol on inflammatory responses and gut barrier function. The results showed that eugenol pre-treatment significantly suppressed the LPS-stimulated interleukin 8 (IL-8) level and the mRNA abundance of tumor necrosis factor α (TNF-α); restored the LPS-stimulated decrease of mRNA abundance of tight junction proteins zonula occludens-1 (ZO-1), occludin (OCLN) and the mRNA abundance of nutrient transporters B0-system neutral amino acid co-transporter (B0AT1), system ASC sodium-dependent neutral amino acid exchanger 2 (ASCT2), apical sodium-dependent glucose transporter 1 (SGLT1), excitatory amino acid transporter 1 (EAAC1) and peptide transporter 1 (PepT1). In addition, eugenol improved the expression and even redistribution of ZO-1 and tended to increase TEER value and maintained the barrier integrity. In conclusion, a low dose of eugenol attenuated inflammatory responses and enhanced selectively permeable barrier function during LPS-induced inflammation in the IPE-J2 cell line.
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Animal Science
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