Protective effects of silymarin against diquat-induced hepatitis in layer by inhibiting oxidative stress and TLR4/MyD88/NF-κB signaling pathway.

Diquat is a widely utilized bipyridine herbicide; inadvertent exposure to it can result in detrimental effects on both animal and human health, particularly causing liver damage. The objective of this research was to examine the protective properties of silymarin against diquat-induced inflammatory damage in the liver of layers by alleviating oxidative stress and inhibiting the TLR4/MyD88/NF-κB signaling pathway. Histopathological analysis revealed inflammatory lesions and significantly elevated histological inflammation scores in hepatic tissues 24 h after diquat exposure. Diquat exposure elevated MDA levels and GSH-Px, reduced T-AOC, and disrupted antioxidant enzymes in serum and liver, thereby inducing oxidative stress. This upregulation was observed in both mRNA and protein expression levels of IL-1β, IL-6, TNF-α, TLR4, MyD88, and NF-κB (p65 and IκB), indicating that diquat exposure activated the TLR4/MyD88/NF-κB signaling pathway, resulting in hepatic inflammatory injury. The addition of silymarin effectively attenuated these molecular upregulations induced by diquat exposure. In conclusion, diquat induces oxidative stress in the liver of layers and triggers the activation of the TLR4/MyD88/NF-κB signaling pathway, thereby initiating hepatitis in layers. Silymarin exerts a protective effect against diquat-induced liver damage in layers by attenuating oxidative stress and suppressing the TLR4/MyD88/NF-κB signaling pathway.