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

文献类型： 外文期刊

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 ;

作者机构： 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

关键词： alanyl-glutamine; bovine intestinal cell; lipopolysaccharide; inflammation; intestinal barrier function

期刊名称：BIOCHEMISTRY AND CELL BIOLOGY （ 影响因子：3.626； 五年影响因子：3.178 ）

ISSN： 0829-8211

年卷期： 2019 年 97 卷 6 期

页码：

收录情况： SCI

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.

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