Rutin modified selenium nanoparticles reduces cell oxidative damage induced by H2O2 by activating Nrf2/HO-1 signaling pathway

Oxidative damage of neurons is one of the key pathological markers of Alzheimer's disease (AD), which eventually leads to neuronal apoptosis and loss. Nuclear factor E2-related factor 2 (Nrf2) is a key regulator of antioxidant response and is considered to be an important therapeutic target for neurodegenerative diseases. In this study, the selenated derivative of antioxidant rutin (Se-Rutin) was synthesized with sodium selenate (Na₂SeO₃) as raw material by a simple electrostatic-compound in situ selenium reduction method. The effects of Se-Rutin on H₂O₂ induced oxidative damage in Pheochromocytoma PC12 cells were evaluated by cell viability, apoptosis, reactive oxygen species level and the expression of antioxidant response element (Nrf2). The results showed that H₂O₂ treatment significantly increased the level of apoptosis and reactive oxygen species, while the level of Nrf2 and HO-1 decreased. However, Se-Rutin significantly reduced H₂O₂ induced apoptosis and cytotoxicity, and increased the expression of Nrf2 and HO-1, both of which were better than that of pure rutin. Therefore, the activation of Nrf2/HO-1 signaling pathway may be the basis of Se-Rutin's anti-oxidative damage to AD.