Bioactive constituents from cinnamon, hemp seed and polygonum cuspidatum protect against H(2)O(2) but not rotenone toxicity in a cellular model of Parkinson's disease

Mitochondrial dysfunction and oxidative stress are two factors that are thought to contribute to the pathogenesis of Parkinson's disease (PD), a debilitating progressive neurodegenerative disorder that results in the loss of catecholamine producing cells throughout specific regions of the brain. In this study we aimed to compare the effects of hydrogen peroxide (H(2)O(2)) and rotenone (a pesticide and mitochondrial complex 1 inhibitor) on cell viability and the expression of tyrosine hydroxylase (TH) in a cellular model of PD. We also sought to investigate the potential neuroprotective benefits of bioactive constituents from cinnamon, hemp seed and polygonum cuspidatum. To create a model, SH-SY5Y cells transfected with human TH isoform 1 were treated with varying concentrations of H(2)O(2) and rotenone, in the presence or absence of bioactive constituents. The effect of these toxins and constituents on cell viability, apoptosis and protein expression was assessed using MTT viability assays and western blotting. Rotenone treatment caused a significant decrease in cell viability but a significant increase in TH in the remaining cells. H(2)O(2) treatment caused a significant decrease in cell viability but had no significant effect on TH expression. Curcumin, cinnamaldehyde, caffeoyltyramide (hemp seed extract) and piceatannol glucoside (polygonum cuspidatum extract) were unable to attenuate rotenone induced cell death, however they were able to provide protection against H(2)O(2) induced cell death. This is the first study to demonstrate the neuroprotective properties of cinnamaldehyde, caffeoyltyramide and piceatannol glucoside in a dopaminergic cell line in response to H(2)O(2).