Curcumin Alleviates Aflatoxin B₁-Induced Liver Pyroptosis and Fibrosis by Regulating the JAK2/NLRP3 Signaling Pathway in Ducks

Abstract

Aflatoxin B1 (AFB1) is a serious pollutant in feed and food which causes liver inflammation, fibrosis, and even cirrhosis. The Janus kinase 2 (JAK2)/signal transducers and activators of the transcription 3 (STAT3) signaling pathway is widely involved in inflammatory response and promotes the activation of nod-like receptor protein 3 (NLRP3) inflammasome, thus leading to pyroptosis and fibrosis. Curcumin is a natural compound with anti-inflammatory and anti-cancer properties. However, whether AFB1 exposure leads to the activation of the JAK2/NLRP3 signaling pathway in the liver and whether curcumin can regulate this pathway to influence pyroptosis and fibrosis in the liver remains unclear. In order to clarify these problems, we first treated ducklings with 0, 30, or 60 µg/kg AFB1 for 21 days. We found that AFB1 exposure caused growth inhibition, liver structural and functional damage, and activated JAK2/NLRP3-mediated liver pyroptosis and fibrosis in ducks. Secondly, ducklings were divided into a control group, 60 µg/kg AFB1 group, and 60 µg/kg AFB1 + 500 mg/kg curcumin group. We found that curcumin significantly inhibited the activation of the JAK2/STAT3 pathway and NLRP3 inflammasome, as well as the occurrence of pyroptosis and fibrosis in AFB1-exposed duck livers. These results suggested that curcumin alleviated AFB1-induced liver pyroptosis and fibrosis by regulating the JAK2/NLRP3 signaling pathway in ducks. Curcumin is a potential agent for preventing and treating liver toxicity of AFB1.

Keywords

• dietary curcumin
• AFB₁ exposure
• hepatocyte pyroptosis
• liver fibrosis
• Jinding duck