Dietary curcumin alleviates aflatoxin B ₁ ‐induced liver injury and improves growth performance in broilers via Nrf2 activation and NLRP3 inflammasome inhibition

BACKGROUND Aflatoxin B 1 (AFB 1 ), 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 AFB 1 ‐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 AFB 1 . 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 AFB 1 diets supplemented with CUR (100, 300, or 500 mg kg −1 ) for 42 days. AFB 1 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 AFB 1 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 AFB 1 ‐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.