4.7 Article

Evaluation of Hepatic Detoxification Effects of Enteromorpha prolifera Polysaccharides against Aflatoxin B1 in Broiler Chickens

期刊

ANTIOXIDANTS
卷 11, 期 9, 页码 -

出版社

MDPI
DOI: 10.3390/antiox11091757

关键词

aflatoxin B-1; hepatotoxicity; detoxification; seaweed polysaccharides; Enteromorpha prolifera; natural antioxidants

资金

  1. Natural Science Foundation of Guangdong Province, China [2022A1515010496]

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The results of this study showed that dietary seaweed-derived polysaccharides (SDP) could alleviate AFB(1)-induced liver toxicity in broilers. This was achieved by inhibiting phase I detoxification enzymes and upregulating the p38MAPK/Nrf2-mediated phase II detoxification enzyme pathway.
Aflatoxin B-1 (AFB(1)) is a major risk factor in animal feed. Seaweed (Enteromorpha prolifera)-derived polysaccharides (SDP) are natural antioxidants with multiple biological functions, which may have an in vivo detoxification effect on AFB(1). The current study aimed to evaluate whether SDP could mitigate AFB(1)-induced hepatotoxicity in broilers. A total of 216 chickens (male, 5 weeks old) were randomly allocated to three groups with differing feeding patterns, lasting 4 weeks: (1) control group (CON, fed a basal diet); (2) AFB(1) group (fed a basal diet mixed with 0.1 mg/kg AFB(1)); and (3) AFB(1) + SDP group (AFB(1) group + 0.25% SDP). The results showed that dietary SDP improved the liver function-related biochemical indicators in serum, and reversed the increase in relative liver weight, hepatic apoptosis and histological damage of broilers exposed to AFB(1). SDP treatment also reduced the activity and mRNA expression of phase I detoxification enzymes, while increasing the activity and mRNA expression of phase II detoxification enzymes in the livers of AFB(1)-exposed broilers, which was involved in the activation of p38 mitogen-activated protein kinase (p38MAPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. In conclusion, dietary SDP alleviated AFB(1)-induced liver injury of broilers through inhibiting phase I detoxification enzymes and upregulating p38MAPK/Nrf2-mediated phase II detoxification enzymes pathway.

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