Alanyl-glutamine ameliorates lipopolysaccharide-induced inflammation and barrier function injury in bovine jejunum epithelial cells

被引:14
作者
Zhang, Xianglun [1 ]
Tan, Xiuwen [1 ]
Liu, Yifan [1 ]
You, Wei [1 ]
Liu, Guifen [1 ]
Liu, Xiaomu [1 ]
Jin, Qing [1 ]
Wei, Chen [1 ]
Wan, Fachun [1 ,2 ]
Zhao, Hongbo [1 ]
机构
[1] Shandong Acad Agr Sci, Shandong Prov Engn Technol Ctr Anim Hlth Breeding, Inst Anim Sci & Vet Med,Shandong Key Lab Anim Dis, Shandong Prov Testing Ctr Beef Cattle Performance, Jinan 250100, Peoples R China
[2] Shandong Normal Univ, Coll Life Sci, Jinan 250114, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
alanyl-glutamine; bovine intestinal cell; lipopolysaccharide; inflammation; intestinal barrier function; NF-KAPPA-B; TIGHT JUNCTION PROTEINS; SIGNALING PATHWAY; TNF-ALPHA; ACTIVATION; EXPRESSION; DISEASE;
D O I
10.1139/bcb-2018-0320
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of this study was to investigate the effects of alanyl-glutamine (Ala-Gln) on the regulation of lipopolysaccharide (LPS)-induced inflammation and barrier function in bovine jejunum epithelial cells (BJECs). BJECs were exposed (or not) to 1 mu g/mL LPS for 24 h to generate a pro-inflammatory model. The cells were then treated with different concentrations of Ala-Gln (0.25, 0.5, 1.0, 2.0, or 4.0 mmol/L) to detect any regulatory effects on the inflammation and barrier function of BJECs. LPS decreased cell viability and enhanced the production of the pro-inflammatory cytokines interleukin (IL)-6 and IL-8. LPS induced inflammation and damaged the barrier function of BJECs, as evidenced by up-regulated mRNA and protein expression of inflammatory factors and down-regulated expression of tight junction proteins. Conversely, Ala-Gln rescued the decrease in cell viability and prevented the accumulation of ILs after LPS exposure by reducing the mRNA and protein expression levels of inflammatory factors. In addition, Ala-Gln induced the mRNA and protein expression of multiple tight junction proteins, and thus reconstituted the barrier function of BJECs. In conclusion, Ala-Gln attenuates injury from inflammation and repairs damaged intestinal barrier induced with LPS, suggesting its potential as a therapeutic agent against intestinal inflammation in mammals.
引用
收藏
页码:670 / 680
页数:11
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