Schematic presentation of the proposed mechanistic basis for the neuroprotective effects of ORF against H
-induced neurotoxicity in human differentiated SH-SY5Y cells. Oxidative stress likely activates pro-apoptotic genes (i.e. JNK, TNF, ING3, BAK1, BAX, p21 and caspase-9) and downregulates anti-apoptotic genes (i.e. ERK1/2, AKT1 and NF-Kβ), resulting in cellular apoptosis. In contrast, ORF likely upregulate endogenous antioxidant defences (i.e. Catalase, SOD1 and SOD2) that can enhance cell survival. Additionally, ORF may downregulate pro-apoptotic genes thereby preventing mitochondrial malfunction and caspase activation. Activation of anti-apoptotic genes likely also contributes to enhanced cell survival.