Tea tree oil attenuates diquat-induced hepatotoxicity in chickens via suppression of the NF-κB-mediated inflammatory pathway.

Exposure to diquat (DIQ) is associated with multi-organ toxicity in humans and animals. This study evaluated the protective role of tea tree oil (TTO) against DIQ-induced hepatotoxicity in chickens and explored its mechanistic basis. 240 one-day-old Hy-Line W-36 chickens were randomly allocated into four groups with 6 replicates per group and 10 birds per replicate. The chickens received either a basal diet or a TTO-supplemented diet (200 ppm) administered via drinking water. On day 20, half of the chickens in each dietary group were administered diquat (DIQ) via intraperitoneal injection (20 mg/kg BW), while the remaining received PBS. DIQ challenge significantly impaired growth performance, as reflected by reduced average daily weight gain, and increased relative liver weight (p < 0.05). It also compromised hepatic antioxidant function, as evidenced by decreased levels of T-AOC, CAT, and GSH-Px, along with elevated MDA levels (p < 0.001). Furthermore, DIQ upregulated the expression of NF-κB, iNOS, COX-2, PTGE, and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) (p < 0.001). TTO supplementation via drinking water counteracted these effects, improving growth metrics, enhancing antioxidant capacity, attenuating lipid peroxidation, and suppressing NF-κB-driven inflammation (p < 0.001). In conclusion, TTO alleviates DIQ-induced liver injury by reinforcing antioxidant defenses and suppressing the NF-κB/iNOS/COX-2 signaling axis, supporting its potential as a natural feed additive to counteract DIQ toxicity in poultry.