Attenuation of H2O2-induced neuronal cell damage by piceatannol

- Piceatannol improves glutathione peroxidases activity as well as its expression.
- Piceatannol sustains expression of SIRT1 and seladin-1 on constant level.
- Piceatannol significantly abolished the H2O2-induced cell damage.

The pathogenesis of neurodegenerative diseases involves oxidative stress-induced cell death. It's well documented that polyphenolic compounds protect neurons against this type of cell damage. Among many polyphenols, stilbenoids derivatives are of particular interest given their potential for use in therapeutics and prevention of neurodegenerative disorders. Piceatannol, which is ubiquitous in variety of edible plants has broad spectrum of action including antioxidant, anti-inflammatory, anti-cancer, and neuroprotective activities. In the present study, the effects of piceatannol against oxidative stress-induced cell damage in neuroblastoma cells were evaluated. Our data indicate that protective effect of piceatannol in neuroblastoma cells under oxidative stress conditions is associated with increased activity and expression of glutathione peroxidase enzymes. Piceatannol also stimulates BDNF, which is involved in neurite outgrowth and maintenance of function in neuronal cells. Furthermore, piceatannol promotes cell survival by sustaining level of sirtuin 1 and seladin-1 mRNA on constant level.