Oleocanthal alleviated lipopolysaccharide-induced acute lung injury in chickens by inhibiting TLR4/NF-κB pathway activation

This study aimed to investigate the ameliorative effect of oleocanthal (OC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in chickens and its possible mechanisms. In total, 20 chickens were randomly divided into 4 groups: control (CON) group, LPS group, LPS + OC group, and OC group. LPS + OC and OC groups were intragastrically administered a 5 mg/kg.d OC dose for 7 d. On d 8, the LPS group and LPS + OC group were intratracheally administered 2 mg/kg LPS for 12 h. It was found that OC ameliorated the pathological morphology and significantly suppressed apoptosis after OC treatment in LPS-induced ALI chicken (P < 0.01). Antioxidant capacity was higher in the LPS + OC group compared with the LPS group (P < 0.01). OC downregulated the related genes and proteins expression of toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-kappa B) pathway in LPS group (P < 0.01). In conclusion, OC supplementation can alleviate LPS-induced ALI in chickens by suppressing apoptosis, enhancing lung antioxidant capacities and inhibiting TLR4/NF-kappa B pathway activation.

Automated summary

This study aimed to investigate the ameliorative effect of oleocanthal (OC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in chickens and its possible mechanisms. The results showed that OC treatment improved the pathological morphology and suppressed apoptosis in LPS-induced ALI chickens. OC supplementation also enhanced antioxidant capacity and inhibited the activation of the toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-κB) pathway in LPS group. Overall, OC supplementation can alleviate LPS-induced ALI in chickens by suppressing apoptosis, enhancing lung antioxidant capacities, and inhibiting TLR4/NF-κB pathway activation.