Effects of compound probiotics and aflatoxin-degradation enzyme on alleviating aflatoxin-induced cytotoxicity in chicken embryo primary intestinal epithelium, liver and kidney cells
文献类型： 外文期刊
第一作者： Guo, Hong-Wei
作者： Guo, Hong-Wei;Chang, Juan;Wang, Ping;Yin, Qing-Qiang;Liu, Chao-Qi;Xu, Xiao-Xiang;Dang, Xiao-Wei;Hu, Xiao-Fei;Wang, Quan-Liang
作者机构：
关键词： Aflatoxin B-1; Compound probiotics; Mycotoxin-degradation enzyme; Chicken embryo primary cells; Cell damage alleviation
期刊名称：AMB EXPRESS （ 影响因子：3.298； 五年影响因子：3.427 ）
ISSN： 2191-0855
年卷期： 2021 年 11 卷 1 期
页码：
收录情况： SCI
摘要： Aflatoxin B-1 (AFB(1)) is one of the most dangerous mycotoxins for humans and animals. This study aimed to investigate the effects of compound probiotics (CP), CP supernatant (CPS), AFB(1)-degradation enzyme (ADE) on chicken embryo primary intestinal epithelium, liver and kidney cell viabilities, and to determine the functions of CP+ADE (CPADE) or CPS+ADE (CPSADE) for alleviating cytotoxicity induced by AFB(1). The results showed that AFB(1) decreased cell viabilities in dose-dependent and time-dependent manners. The optimal AFB(1) concentrations and reactive time for establishing cell damage models were 200 mu g/L AFB(1) and 12 h for intestinal epithelium cells, 40 mu g/L and 12 h for liver and kidney cells. Cell viabilities reached 231.58% (p<0.05) for intestinal epithelium cells with CP addition, 105.29% and 115.84% (p<0.05) for kidney and liver cells with CPS additions. The further results showed that intestinal epithelium, liver and kidney cell viabilities were significantly decreased to 87.12%, 88.7% and 84.19% (p<0.05) when the cells were exposed to AFB(1); however, they were increased to 93.49% by CPADE addition, 102.33% and 94.71% by CPSADE additions (p<0.05). The relative mRNA abundances of IL-6, IL-8, TNF-alpha, iNOS, NF-kappa B, NOD1 (except liver cell) and TLR2 in three kinds of primary cells were significantly down-regulated by CPADE or CPSADE addition, compared with single AFB(1) group (p<0.05), indicating that CPADE or CPSADE addition could alleviate cell cytotoxicity and inflammation induced by AFB(1) exposure through suppressing the activations of NF-kappa B, iNOS, NOD1 and TLR2 pathways.
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