Regulatory mechanism of quercitrin on oxidative stress and histone acetylation changes in PRV infected 3D4/2 cells.

Viral infection causes oxidative stress damage to the body. Quercitrin is a flavonoid compound that exists widely in many plants and it exhibits antioxidant properties. The aim of this work was to investigate the antioxidant mechanism of quercitrin and its effect on histone acetylation changes. 3D4/2 cells were infected by PRV (Pseudorabies virus) with or without quercitrin, cell viability and antioxidant enzyme activity were tested. In addition, oxidative stress-related signaling pathways and histone acetylation changes were analyzed by western blots. The results showed that quercitrin played a protective effect on PRV infected 3D4/2 cells, the effects of quercitrin on the activity of SOD (Superoxide Dismutase), GPx (Glutathione peroxidase), CAT (Catalase) in PRV infected cell were not the same, quercitrin could increase the proteins expression levels AcH3, AcH4 and Nrf2 signaling pathway related proteins of PRV infected cells at certain concentrations. In addition, quercitrin could inhibit AKT phosphorylation in PRV infected cells and further promote the phosphorylation levels of AMPK and PPAR-γ protein expression levels. Moreover, AMPK pathway inhibitors blocked the promoting effect of quercitrin on Nrf2 and HO1 protein expression levels; PPAR-γ inhibitors blocked the promoting effect of quercitrin on Nrf2. The findings demonstrated that quercitrin could regulate histone acetylation in PRV infected 3D4/2 cells through the Nrf2 pathway and quercitrin could alleviate oxidative stress in 3D42 cells induced by PRV, which is associated with the Nrf2, AMPK, and PPAR-γ signaling pathway.