Rutin modified selenium nanoparticles reduces cell oxidative damage induced by H

Area of Science:

• Neuroscience
• Biochemistry
• Pharmacology

Background:

• Oxidative neuronal damage is a hallmark of Alzheimer's disease (AD), leading to apoptosis and cell loss.
• Nuclear factor E2-related factor 2 (Nrf2) is a critical regulator of the antioxidant response and a potential therapeutic target for neurodegenerative diseases.

Purpose of the Study:

• To synthesize a novel selenated derivative of rutin (Se-Rutin).
• To evaluate the protective effects of Se-Rutin against hydrogen peroxide (H2O2)-induced oxidative damage in PC12 cells.
• To investigate the underlying mechanism involving the Nrf2/HO-1 signaling pathway.

Main Methods:

• Se-Rutin synthesized using sodium selenate and rutin via in situ selenium reduction.
• PC12 cells exposed to H2O2 to induce oxidative stress.
• Assessed cell viability, apoptosis, reactive oxygen species (ROS) levels, and Nrf2/HO-1 expression.

Main Results:

• H2O2 treatment increased apoptosis and ROS, while decreasing Nrf2 and HO-1 expression.
• Se-Rutin significantly reduced H2O2-induced apoptosis and cytotoxicity.
• Se-Rutin treatment enhanced Nrf2 and HO-1 expression, outperforming pure rutin.

Conclusions:

• Se-Rutin demonstrates potent antioxidant and neuroprotective effects against oxidative stress.
• The activation of the Nrf2/HO-1 signaling pathway is identified as the mechanism underlying Se-Rutin's protective effects.
• Se-Rutin represents a promising therapeutic agent for Alzheimer's disease and other neurodegenerative conditions.