Tea tree oil inhibits hydrogen sulfide-induced oxidative damage in chicken lungs through CYP450s/ROS pathway

A large amount of hydrogen sulfide (H₂S) is produced in the process of chicken breeding, which can cause serious inflammation and oxidative damage to the respiratory system of chickens. Tea tree oil (TTO) has antioxidant and anti-inflammatory properties. No studies have been reported on the use of TTO in H₂S-induced lung injury in chickens. Therefore, in this study, 240 one-day-old Roman pink laying hens were randomly and equally divided into 3 groups: control group (CON), H₂S exposure group (AVG, containing H₂S), and TTO treatment group (TTG, containing H₂S and 0.02 mL/L TTO) to establish an experimental model of TTO treatment with H₂S exposure for a period of 42 d. Hematoxylin and eosin (H&E) staining was used to detect lung histopathology. Gene expression profiles were analyzed using transcriptomics. The underlying mechanism of the amelioration of lung injury by TTO was further revealed by antioxidant enzyme assays and qRT-PCR. The results showed that H₂S exposure induced significant gene expression of CYP450s (CYP1B1 and CYP1C1) (P < 0.05), and caused intense oxidative stress, apoptosis and inflammation compared with CON. TTO could reduce ROS production and enhance antioxidant capacity (SOD, CAT, T-AOC, and GSH-PX) by regulating the CYP450s/ROS pathway (P < 0.05). Compared with the control group, the treatment group showed significantly decreased expression of apoptotic (Caspase-8, Caspase-3, Bid and Fas) (P < 0.05) and inflammatory (IL-4, IL-16, NF-κB, TNF-α and IFN-γ) (P < 0.05) factors in the lung. This study revealed that TTO regulated CYP450s/ROS pathway to alleviate H₂S-induced lung injury in chickens. These results enrich the theory of the action mechanism of TTO on H₂S-exposed chicken lungs and are of great value for the treatment of H₂S-exposed animals.