Fig. 5

Acetylated HMGB1 contributes to interact with GPX4 to regulate ROS levels and inflammation. a Pulldown assay was performed to further prove that HMGB1 interacted with the GPX4 in SW480 and HCT116 cells. b IP results revealed that LPS elevated the acetylation levels of HMGB1 and acetylated HMGB1 was responsible for the interaction between HMGB1 and GPX4. c Western blot results indicated leptomycin B (an inhibitor of nuclear export) prevented HMGB1 translocation. d Western blot results showed that Res administration blocked HMGB1 nucleocytoplasmic translocation with increased Sirt1 expression. e IP results showed Res weakened the interaction of HMGB1 and GPX4. Our data sought to examined the connection between Res and ROS levels/NF-kB and the results indicated that Res effectively inhibited the levels of ROS (f) and p-IKBα and p-p65 protein expressions (g) elevated by LPS. Res, resveratrol