Curcumin attenuates aflatoxin B1-induced ileum injury in ducks by inhibiting NLRP3 inflammasome and regulating TLR4/NF-κB signaling pathway

被引:7
作者
Pan, Hang [1 ,2 ]
Hu, Ting [1 ]
He, Ying [3 ,4 ,5 ]
Zhong, Gaolong [1 ]
Wu, Shaofeng [1 ]
Jiang, Xuanxuan [1 ]
Rao, Gan [1 ]
You, Yanli [2 ]
Ruan, Zhiyan [6 ]
Tang, Zhaoxin [1 ]
Hu, Lianmei [1 ]
机构
[1] South China Agr Univ, Coll Vet Med, Guangzhou 510642, Peoples R China
[2] Yantai Univ, Coll Life Sci, Yantai 264005, Shandong, Peoples R China
[3] Guangxi Vet Res Inst, Guangxi Key Lab Vet Biotechnol, Nanning 530001, Peoples R China
[4] Guangxi Key Lab Vet Biotechnol, Nanning, Guangxi, Peoples R China
[5] Minist Agr & Rural Affairs China, Key Lab China Guangxi ASEAN Cross Border Anim Dis, Nanning, Peoples R China
[6] Guangdong Food & Drug Vocat Coll, Sch Pharm, 321 Longdong North Rd, Guangzhou 510520, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Aflatoxin B1; Curcumin; Intestinal microbiota; Pyroptosis; Intestinal barrier; Inflammation; GROWTH-PERFORMANCE; GUT MICROBIOTA; TNF-ALPHA; CELL; B-1; SUPPLEMENTATION; MODULATION; FOOD;
D O I
10.1007/s12550-024-00524-7
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Aflatoxin B1 (AFB1) is a widespread toxic contamination in feed for animals. The primary active component of turmeric, curcumin (Cur), is an antioxidant and an anti-inflammatory. However, it is yet unknown how AFB1 affects the intestinal epithelial barrier and whether Cur acts as a protective mechanism when exposed to AFB1. Here, we explored the mechanism of AFB1-induced intestinal injury from intestinal epithelial barrier, inflammation, pyroptosis, and intestinal flora, and evaluated the protective role of Cur. We found that AFB1 caused weight loss and intestinal morphological damage that is mainly characterized by shortened intestinal villi, deepened crypts, and damaged intestinal epithelium. Exposure to AFB1 decreased the expression of Claudin-1, MUC2, ZO-1, and Occludin and increased the expression of pyroptosis-related factors (NLRP3, GSDMD, Caspase-1, IL-1 beta, and IL-18) and inflammation-related factors (TLR4, NF-kappa B, I kappa B, IFN-gamma, and TNF-alpha). Furthermore, ileal gut microbiota was altered, and simultaneously, the Lactobacillus abundance was decreased. The gut microbiota interacts with a wide range of physiologic functions and disease development in the host through its metabolites, and disturbances in gut microbial metabolism can cause functional impairment of the ileum. Meanwhile, Cur can ameliorate histological ileum injuries and intestinal flora disturbance caused by AFB1. We found that Cur reversed the effects of AFB1 through modulating both NLRP3 inflammasome and the TLR4/NF-kappa B signaling pathway. In conclusion, AFB1 can induce inflammatory damage and pyroptosis in duck ileum, while Cur has obviously protective effects on all the above damages.
引用
收藏
页码:255 / 268
页数:14
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