Lactobacillus bulgaricus or Lactobacillus rhamnosus Suppresses NF-κB Signaling Pathway and Protects against AFB1-Induced Hepatitis: A Novel Potential Preventive Strategy for Aflatoxicosis?

Aflatoxin B₁ (AFB₁), a mycotoxin found in food and feed, is immunotoxic to animals and poses significant threat to the food industry and animal production. The primary target of AFB₁ is the liver. To overcome aflatoxin toxicity, probiotic-mediated detoxification has been proposed. In the present study, to investigate the protective effects and molecular mechanisms of <i>Lactobacillus bulgaricus</i> or <i>Lactobacillus rhamnosus</i> against liver inflammatory responses to AFB₁, mice were administered with AFB₁ (300 μg/kg) and/or <i>Lactobacillus</i> intragastrically for 8 weeks. AML12 cells were cultured and treated with AFB₁, BAY 11-7082 (an NF-κB inhibitor), and different concentrations of <i>L. bulgaricus</i> or <i>L. rhamnosus.</i> The body weight, liver index, histopathological changes, biochemical indices, cytokines, cytotoxicity, and activation of the NF-κB signaling pathway were measured. AFB₁ exposure caused changes in liver histopathology and biochemical functions, altered inflammatory response, and activated the NF-κB pathway. Supplementation of <i>L. bulgaricus</i> or <i>L. rhamnosus</i> significantly prevented AFB₁-induced liver injury and alleviated histopathological changes and inflammatory response by decreasing NF-κB p65 expression. The results of in vitro experiments revealed that <i>L.</i><i>rhamnosus</i> evidently protected against AFB₁-induced inflammatory response and decreased NF-κB p65 expression when compared with <i>L. bulgaricus</i>. These findings indicated that AFB₁ exposure can cause inflammatory response by inducing hepatic injury, and supplementation of <i>L. bulgaricus</i> or <i>L. rhamnosus</i> can produce significant protective effect against AFB₁-induced liver damage and inflammatory response by regulating the activation of the NF-κB signaling pathway.