Inhibition of aflatoxin B1-induced murine hepatocyte pyroptosis by Bacillus amyloliquefaciens by activation of the Nrf2/HO-1 pathway.

Human and animals are continuously exposed to variable levels of mycotoxin that occur naturally in the diet. Aflatoxin B1 (AFB1) is the most toxic and carcinogenic aflatoxin. Probiotics have a vital role in mycotoxin detoxification. The objective of this study was to investigate potential protective effects of probiotics Bacillus amyloliquefaciens and its mechanism. In in vitro experiments, exposure of AML-12 cells to AFB1 reduced cell viability, increased oxidative stress, and induced cell pyroptosis. Additionally, there was down-regulation of Nuclear factor erythropoietin-2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) expression. Importantly, Nrf2siRNA exacerbated AFB1-induced cell pyroptosis, whereas overexpression of Nrf2 alleviated it. Furthermore, Bacillus amyloliquefaciens reversed the upregulated cell pyroptosis, and downregulated Nrf2/HO-1 induced by AFB1. Interestingly, Nrf2 siRNA abolished the protective effect exerted by Bacillus amyloliquefaciens, whereas overexpression of Nrf2 had the opposite effect. In in vivo experiments, AFB1 caused liver impairment, oxidative stress and cell pyroptosis, whereas Bacillus amyloliquefaciens exerts its protective effect via Nrf2/HO-1 signaling in AFB1-induced deleterious effects. In summary, Bacillus amyloliquefaciens may regulate the Nrf2/HO-1 signaling pathway to mitigate AFB1-induced cell pyroptosis, thereby providing a potential therapeutic intervention for mycotoxicosis associated with AFB1-induced hepatic injury.