Abstract: Objective: This study was focused on the protective effect of curcumin on cellular oxidative damage and cell apoptosis induced by Cu2＋ in human neuroblastoma SH-SY5Y cells transfected by human amyloid-β precursor protein (APP) (SH-SY5Y-APP695). Methods: SH-SY5Y-APP695 cells were treated with 50 μmol/L Cu2＋ at 37 ℃ for 24 h with or without curcumin pre-protection. Cell viability was detected by cell counting kit-8 (CCK-8). Extracellular lactate dehydrogenase (LDH), intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were determined by commercial assay kits. The enzymatic activities of caspase-3, caspase-8 and caspase-9 were assessed. Phosphorylation levels of NF-E2-related factor 2 (Nrf2) at Ser-40 (pSer40-Nrf2) and HO-1 were detected by Western blot analysis. Results: Compared with the control group, Cu2＋ administration led to decreased cell viability and mitochondrial membrane potential, increased levels of LDH, intracellular ROS and caspase-3, caspase-8 and caspase-9 activities, and elevated levels of pSer40-Nrf2 and HO-1. Conversely, curcumin increased cell viability and mitochondrial membrane potential, decreased the levels of LDH and intracellular ROS, significantly mitigated caspase-9 and caspase-3 activities, and reduced the expression levels pSer40-Nrf2 and HO-1. Conclusion: Curcumin can attenuate Cu2＋-induced cellular oxidative damage and cell apoptosis.

Key words: Alzheimer’s disease, Cu2+, oxidative damage, cell apoptosis, curcumin, Nrf2-antioxidant response element pathway