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.

氧化应激介导的神经元损伤被认为是神经退行性疾病发病机制和发展的重要因素。尽管β-细辛脑以其神经保护药理特性而广为人知，但β-细辛脑抗氧化应激的确切机制尚未完全阐明。本研究的目的是研究 β-细辛醚抗 PC12 细胞氧化损伤的潜在机制。我们的研究结果表明，β-细辛醚处理通过增加超氧化物歧化酶 (SOD) 的活性，显着缓解了细胞活力的降低和乳酸脱氢酶 (LDH)、丙二醛 (MDA) 和活性氧 (ROS) 的过度积累，过氧化氢酶 (CAT) 和谷胱甘肽 (GSH)。而且，β-细辛醚预处理还激活了核因子 2 红细胞相关因子 2 (Nrf2) 及其下游靶标血红素加氧酶-1 (HO-1)，后者参与淬灭活性氧以抑制氧化应激。此外，当被 Nrf2 siRNA 沉默时，β-细辛脑的保护作用降低，H 诱导的氧化应激₂ O ₂增强。总之，我们的研究结果表明，β-细辛脑可以通过激活 PC12 细胞中的 Nrf2/HO-1 通路来减少氧化应激，突出了 β-细辛脑在神经退行性疾病中的潜在治疗作用。