Abstract: To determine the neuroprotective effects of seed watermelon polysaccharide on PC12 cells injured by H₂O₂ and the molecular mechanisms underlying these neuroprotective effects.The cell viability was analyzed by CCK-8 assay,the toxicity model was established by treating PC12 cells with H₂O₂.The releasing rate of LDH was determined by the color reaction of diaphorase INT.ROS production was determined by DCFH-DA fluorescence.8-OHdG production was determined by ELISA.Mitochondria membrane potential was determined by JC-1 staining.Caspase-3 activity was determined by caspase3 catalyze the substrate specificity Ac-DEVD-pNA.Caspase-9 activity was determined by caspase-9 catalyze the substrate specificity Ac-LEHD-pNA.In comparison to control cells,exposure of cells to 500 μmol/L H₂O₂ for 24 h resulted in approximately 65% cell viability of control (P<0.01). H₂O₂ induced significantly the increase of LDH release,intracellular ROS and 8-OHdG (P<0.01),and the decrease of mitochondrial membrane potential (P<0.01). H₂O₂ induced oxidative stress increased caspase-3 and caspase-9 activity (P<0.01).Compared with H₂O₂ group,different doses of SWP can significantly improve the change of the index H₂O₂-induced (P<0.05).Polysaccharide from seed watermelon had protective effect on PC12 cells injury induced by H₂O₂ in culture.

Key words: polysaccharide from seed watermelon, hydrogen peroxide, oxidative damage, caspase, PC12 cells