Arginine-derived carbon dots with antioxidant activity for treating aflatoxin B1-induced liver injury via Nrf2/Keap1 and NLRP3 pathways in mice

Abstract

Aflatoxin B1 (AFB1) is a prevalent contaminant in food and feed matrices, known for its hepatotoxic effects. Its metabolic breakdown generates reactive oxygen species (ROS), leading to oxidative stress and subsequent liver damage. Mitigating oxidative stress is, therefore, essential for ameliorating the hepatocellular damage and systemic toxicity caused by AFB1. Here, we synthesized arginine carbon dots (Arg-CDs) with robust antioxidant properties through a simple hydrothermal method using arginine and citric acid. Our investigation demonstrated that Arg-CDs effectively mitigate oxidative stress in nematodes. Furthermore, in murine models of AFB1-induced hepatic injury, Arg-CDs effectively restored liver function, as evidenced by the improvement in histopathological features and biochemical markers. Notably, Arg-CDs administration upregulated the transcriptional activity of nuclear factor erythroid 2-related factor 2 (Nrf2), along with its downstream antioxidant effectors and phase II detoxifying enzymes under AFB1 exposure. Moreover, Arg-CDs alleviated hepatic inflammatory injury by modulating the NLRP3/Caspase-1/GSDMD-mediated pyroptosis pathway. Arg-CDs also demonstrated therapeutic potential in enhancing intestinal barrier function in AFB1-exposed mice. Collectively, these findings highlight the potential of Arg-CDs as a novel and biocompatible therapeutic modality for alleviating AFB1-induced hepatic and intestinal damage.