Curcumin ameliorates aflatoxin B1-induced brain toxicity in ducks by attenuating inflammation and PANoptosis

Aflatoxin B1 (AFB1) is a highly toxic mycotoxin that poses significant risks to poultry health, causing neurotoxicity and economic losses. However, the precise mechanisms underlying AFB1-induced brain injury, particularly regarding the role of PANoptosis—a coordinated cell death pathway—remain largely unexplored. This study aimed to investigate the mechanisms of AFB1-induced neurotoxicity in ducks, focusing on the inflammatory response and PANoptosis, and to evaluate the potential neuroprotective effects of curcumin. A duck model of AFB1 intoxication was established. Ducks were divided into four groups: Control, Curcumin (Cur), AFB1, and AFB1+Cur. We assessed body weight, brain coefficients, and histopathological changes. Oxidative stress was measured via SOD activity and MDA content. The integrity of the blood-brain barrier (BBB) and the expression of genes and proteins related to the TLR4/NF-κB signaling pathway and PANoptosis were analyzed using Western blot, RT-qPCR, and immunofluorescence. AFB1 exposure resulted in significant growth retardation, degenerative brain damage (such as neuronal necrosis, cytoplasmic vacuolization, and nuclear shrinkage), reduced SOD activity by approximately 53%, and MDA levels increased by approximately 1.88-fold. It also compromised the BBB by downregulating ZO-1 and Occludin expression. Furthermore, AFB1 significantly upregulated the TLR4/NF-κB signaling pathway and key PANoptosis markers (ZBP1, RIPK1/3, Caspase-8, NLRP3, GSDMD). Curcumin attenuated the pathological damage of AFB1-intoxicated duck brain and was able to mitigate AFB1-induced neurotoxicity by inhibiting the phosphorylation of NF-κB and IκB, preventing IκB degradation, and downregulating the expression of key PANoptosis mediators. AFB1 could trigger PANoptosis and activate the TLR4/NF-κB signaling pathway, leading to brain damage in ducks. Curcumin exerted a significant protective effect by inhibiting these pathways, suggesting its potential as a therapeutic agent for alleviating mycotoxin-induced neurological damage.