Polystyrene Nanoparticles Protect Polystyrene Polysaccharide-induced Organ Oxidative Damage in Mice with Liver Cancer by Regulating the Mitogen-activated Protein Kinase/Nuclear Factor Erythroid 2-related Factor 2/Heme Oxygenase 1 (MAPK/Nrf2-HO-1) Signaling Pathway and Upregulating Superoxide Dismutase Expression

Background: Polygonatum polysaccharide has certain limitations in drug delivery and cellular uptake. To overcome these problems, polystyrene nanoparticles serve as an effective carrier to improve its bioavailability and antioxidant effects. Objectives: To this end, we explored the role of polystyrene nanoparticle-mediated polysaccharide complex in liver cancer. Materials and Methods: Polygonatum sibiricum polysaccharide-polystyrene (PSP-PS) nanomaterials were prepared, and liver cancer mouse models were constructed. Antioxidant enzymes and proteins in the mouse spleen and thymus were detected. The levels of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), and total antioxidant capacity (T-AOC) in the mouse spleen and thymus were detected. Western blot detects the expression levels of p38, JNK, and ERK1/2 proteins in the mitogen-activated protein kinase (MAPK) signaling pathway; it also detects the expression levels of Keap1, Nrf-2, and HO-1 proteins in the Nrf-2 and HO-1 signaling pathways. Results: PSP-PS nanomaterials were successfully prepared, and a liver cancer mouse model was successfully constructed. Under the intervention of PSP-PS, MDA in the spleen and thymus of mice decreased, SOD in the spleen and thymus increased, T-AOC in the spleen increased, GSH in the spleen decreased, GSH in the thymus increased, Keap1 in the spleen decreased, Keap1 in the thymus increased, and Keap1 in the spleen and thymus increased. Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) were both elevated in the thymus. p38, JNK, and ERK protein levels in the MAPK signaling pathway were significantly reduced. Conclusion: PSP-PS upregulates SOD expression by inhibiting the MAPK/Nrf2-HO-1 signaling, thereby protecting against oxidative damage to organs in mice with liver cancer.