Objective To explore the mechanism by which procyanidin B₂ (PB2) intervenes in inflammation and insulin resistance (IR) through multi-target modulation.Methods The potential of PB2 in diabetes prevention was evaluated via in vitro antioxidant assays, and molecular biology techniques were used to reveal the regulatory effect of PB2 on the NF-κB inflammatory signaling pathway during the progression of IR.Results PB2 significantly reduced reactive oxygen species (ROS) levels in HepG2 cells by scavenging free radicals and inhibited the expression of inflammatory factors IL-6, IL-1β, and TNF-α. By suppressing the JNK/NF-κB signaling cascade, PB2 blocked excessive ROS production, thereby restoring intracellular redox homeostasis and ultimately improving insulin resistance.Conclusion PB2 can regulate glucose metabolism and antagonize inflammatory responses by modulating redox balance and inflammatory signaling pathways.