丁酸钠
肠道菌群
丁酸盐
基础(医学)
碱性磷酸酶
生物
平衡
内科学
小肠
潘尼斯电池
内分泌学
生物化学
医学
酶
基因
发酵
胰岛素
作者
Shuai Wang,Cong Zhang,Jiacheng Yang,Xu Wang,Kuntan Wu,Beiyu Zhang,Jiacai Zhang,Ao Yang,Shahid Ali Rajput,Desheng Qi
标识
DOI:10.1021/acs.jafc.0c00791
摘要
This study aims to determine whether sodium butyrate (SB) could antagonize deoxynivalenol (DON)-induced intestinal epithelial dysfunction. In a four-week feeding trial, twenty-eight barrows were randomly divided into four treatments: (1) uncontaminated basal diet (control); (2) 4 mg/kg DON-contaminated diet (DON); (3) basal diet supplemented with 0.2% SB (SB); and (4) 4 mg/kg DON + 0.2% SB (DON + SB). A decrease in performance was observed in DON-exposed animals, which was prevented by the dietary SB supplementation. DON exposure also depressed the expression of host defense peptides (HDPs) in the intestine, impaired the intestinal barrier integrity, and disturbed the gut microbiota homeostasis. These alterations induced by DON were attenuated by SB supplementation. The supplementation of 0.2% SB ameliorated the adverse effects of DON on the liver in terms of hepatic lesions as well as serum concentrations of alkaline phosphatase and aspartate aminotransferase. In IPEC-J2 cells, pretreatment with SB alleviated the DON-induced decreased cell viability. Additionally, the NOD2/caspase-12 pathway participated in the alleviation of SB on DON-induced diminished HDP expression. Taken together, these data demonstrated that SB protected piglets from DON-induced intestinal barrier dysfunction potentially through stimulation of intestinal HDP assembly and regulation in gut microbiota.
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