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Eugenol attenuates inflammatory response and enhances barrier function during lipopolysaccharide-induced inflammation in the porcine intestinal epithelial cells.
Journal of Animal Science ( IF 2.7 ) Pub Date : 2020-07-31 , DOI: 10.1093/jas/skaa245
Qianru Hui 1 , Emily Ammeter 1 , Shangxi Liu 1 , Runqiang Yang 1, 2 , Peng Lu 1 , Ludovic Lahaye 3 , Chengbo Yang 1
Affiliation  

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.

中文翻译:


丁子香酚可减轻脂多糖诱导的猪肠上皮细胞炎症反应并增强屏障功能。



丁香酚(4-烯丙基-2-甲氧基苯酚)是一种精油成分,具有抗菌、抗炎和抗氧化特性,但丁香酚对猪肠道炎症的影响尚未得到研究。本研究建立了体外脂多糖( LPS )诱导的猪肠上皮细胞炎症模型( IPEC-J2 )。细胞用 100 μM (16.42 mg/L) 丁子香酚预处理 2 小时,然后用 10 μg/mL LPS 刺激 6 小时。促炎细胞因子的分泌、活性氧、促炎细胞因子的基因表达、紧密连接蛋白和营养转运蛋白、闭合小带-1 ( ZO-1 ) 的表达和分布、跨上皮电阻 ( TEER ) 和细胞测量渗透性以研究丁子香酚对炎症反应和肠道屏障功能的影响。 结果表明,丁子香酚预处理显着抑制LPS刺激的白细胞介素8( IL-8 )水平和肿瘤坏死因子α( TNF- α )的mRNA丰度;恢复 LPS 刺激的紧密连接蛋白zonula occlusionns-1 ( ZO-1 )、occludin ( OCLN ) mRNA 丰度的减少以及营养转运蛋白B 0系统中性氨基酸协同转运蛋白 ( B 0 AT1 ) mRNA 丰度的降低, ASC系统包括钠依赖性中性氨基酸交换器2( ASCT2 )、顶端钠依赖性葡萄糖转运蛋白1( SGLT1 )、兴奋性氨基酸转运蛋白1( EAAC1 )和肽转运蛋白1( PepT1 。此外,丁子香酚改善了ZO-1的表达甚至重新分布,并倾向于增加TEER值并维持屏障完整性。总之,低剂量的丁子香酚可减弱 IPE-J2 细胞系 LPS 诱导炎症期间的炎症反应并增强选择性渗透屏障功能。
更新日期:2020-08-01
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