Abstract: This study developed a cell model of oxidative damage by treating PC12 cells for 24 h with 200 µmol/L H2O2 and determined the degree of oxidative stress by assaying the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and lactate dehydrogenase (LDH) and the level of malondialdehyde (MDA). Moreover, cell apoptosis and reactive oxygen species (ROS) levels were evaluated. Western blot and real-time polymerase chain reaction (PCR) were used to detect the protein and mRNA expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3, nuclear factor E2 related factor 2 (Nrf2), kelch-like ECH-associated protein 1 (Keap1), and heme oxygenase-1 (HO-1). The results showed that after being treated with 200 µmol/L H2O2 for 24 h, the survival rate of PC12 cells was 60.12%. Cytotoxicity experiments showed that nervonic acid could significantly reduce the contents of LDH and MDA, inhibit excessive production of ROS, and enhance the activities of SOD and GSH-Px in H2O2-injuried cells. In addition, it significantly upregulated the expression of Bcl-2, Nrf2 and HO-1, and downregulated the expression of caspase-3, Bax, and Keap1. In summary, nervonic acid has a protective effect on H2O2-induced oxidative damage in PC12 cells by a mechanism associated with the activation of the Nrf2/HO-1 signaling pathway.

Key words: nervonic acid; oxidative damage; PC12 cells; signaling pathway