Dietary curcumin alleviates aflatoxin B1-induced liver injury and improves growth performance in broilers via Nrf2 activation and NLRP3 inflammasome inhibition.

BACKGROUND

Aflatoxin B1 (AFB1), a potent mycotoxin frequently detected in improperly stored poultry feed, induces hepatic oxidative stress, inflammation, and growth retardation in broilers. Curcumin (CUR), a polyphenolic compound derived from Curcuma longa, exhibits strong antioxidant and anti-inflammatory activities; however, its efficacy and mechanisms in mitigating AFB1-induced hepatotoxicity in broilers remain unclear. This study aimed to evaluate the protective effects of dietary CUR supplementation on growth performance and liver health of broilers exposed to AFB1.

RESULTS

A total of 720 broilers (eight replicates of 15 birds each per treatment) were fed a basal diet, an AFB₁-contaminated diet (1 mg kg-1), or AFB1 diets supplemented with CUR (100, 300, or 500 mg kg-1) for 42 days. AFB1 exposure significantly reduced average daily gain and increased feed conversion ratio (P < 0.05), whereas CUR supplementation - particularly 300-500 mg kg-1 - improved growth performance relative to the AFB1 group (P < 0.05). CUR also decreased serum alanine aminotransferase and aspartate aminotransferase activities, alleviated hepatic histopathological damage, enhanced hepatic antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase), and suppressed malondialdehyde accumulation (P < 0.01). At the molecular level, CUR upregulated Nrf2 and its downstream antioxidant genes while downregulating NOD-like receptor protein 3 (NLRP3), caspase-1, and interleukin-1β, indicating attenuation of inflammasome activation and pyroptosis.

CONCLUSION

Dietary curcumin effectively mitigated AFB1-induced hepatotoxicity and performance loss in broilers through activation of the Nrf2 antioxidant pathway and inhibition of the NLRP3 inflammasome. These findings highlight CUR as a promising natural feed additive for protecting poultry against mycotoxin-induced oxidative and inflammatory damage. © 2025 Society of Chemical Industry.