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

Abstract

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.