回肠
抗氧化剂
丁酸钠
势垒函数
体内
微生物学
化学
超氧化物歧化酶
谷胱甘肽
乳酸菌
丁酸盐
生物化学
短链脂肪酸
生物
肠粘膜
内科学
发酵
医学
细胞生物学
酶
生物技术
基因
作者
Jinbiao Zhao,Jinhua Hu,Xi Ma
出处
期刊:Food & Function
[The Royal Society of Chemistry]
日期:2021-01-01
卷期号:12 (20): 9750-9762
被引量:14
摘要
Short-chain fatty acids (SCFA) produced by gut microbial metabolism have been reported to regulate the immunological response and intestinal health of the host by activating G protein-coupled receptors (GPR). It is unclear whether medium-chain fatty acids (MCFA) improve the intestinal barrier function by activating GPR. This study was conducted to investigate the effects of sodium caprylate and sodium butyrate on antioxidant capacity and intestinal barrier function in IPEC-J2 treated with H2O2 and C57/BL6 mouse models. For in vitro and in vivo assays, mice and oxidation-damaged IPEC-J2 (NC) were treated with sodium caprylate (SC) and sodium butyrate (PC) to determine intestinal barrier and antioxidant functions of the host. In vitro, SC treatment increased the concentrations of glutathione and total antioxidant capacity, and expression of claudin-1 and claudin-3 in oxidation-damaged IPEC-J2 (P < 0.05). In vivo, SC treatment improved growth performance, intestinal morphology, expression of claudin-3, and activity of superoxide dismutase in mice (P < 0.05), but decreased interleukin-1β and interferon-γ concentrations in serum compared to the NC group (P < 0.05). Treatment with SC increased the populations of Prevotella_9 in the ileum and Lachnoclostridium and Roseburia in the colon, but decreased the abundances of Streptococcus and Enterococcus in the ileum and Lactobacillus and Clostridium_sensu_stricto_1 in the colon compared with the NC group (P < 0.05). Concentrations of SCFA increased in the SC and PC groups than in the NC group (P < 0.05). Ileal protein expression of GPR 43 in the SC and PC groups was significantly greater than that in the NC group (P < 0.05). In conclusion, our findings confirmed the important role of sodium caprylate in improving intestinal barrier function and gut health by activating GPR 43 through regulating gut microbial metabolism.
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