Oxidative stress-mediated neuron damage is considered an important contributor to the pathogenesis and development of neurodegenerative diseases. Although β-asarone is widely known for its neuroprotective pharmacological properties, the exact mechanism of β-asarone against oxidative stress has not been fully elucidated. The aim of the present study was to investigate underlying mechanisms of β-asarone against oxidative damage in PC12 cells. Our results demonstrated that the treatment of β-asarone significantly alleviated the reduction in cell viability and the excessive accumulation of lactate dehydrogenase (LDH), malondialdehyde (MDA) and reactive oxygen species (ROS) by increasing the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH). Moreover, β-asarone pretreatment also activated nuclear factor 2 erythroid-related factor 2 (Nrf2) and its downstream target heme oxygenase-1 (HO-1), which was involved in quenching reactive oxygen to inhibit oxidative stress. Furthermore, when silenced by Nrf2 siRNA, the protective effect of β-asarone was reduced and the oxidative stress induced by H2O2 was enhanced. In conclusion, our findings revealed that β-asarone could reduce oxidative stress via activating Nrf2/HO-1 pathway in PC12 cells, highlighting the potential therapeutic role of β-asarone in neurodegenerative diseases.
Keywords: Neurotoxicity; Nrf2/HO-1; Oxidative stress; β-Asarone.