Tyrosol exerts a protective effect against dopaminergic neuronal cell death in in vitro model of Parkinson’s disease

• Tyrosol dose and time dependently supresses MPP+-induced cytotoxicity in CATH.a neuron cells.
• MPP+ induced mitochondrial dysfunction and ATP depletion was significantly attenuated by tyrosol.
• Tyrosol treatment upregulated the anti-oxidative enzymes in neurone cells.
• Tyrosol exerts a neuroprotective activity most probably via Akt signalling pathway.

Experimental evidence suggests that tyrosol [2-(4-hydroxyphenyl)ethanol] exhibits potent protective activities against several pathogeneses. In this study, we evaluated the protective effect of tyrosol against 1-methyl-4-phenylpyridinium (MPP+)-induced CATH.a neuron cell death. Tyrosol dose-dependently protected CATH.a cells from MPP+-induced cell death and the protection was more apparent after prolong incubation (48 h). The data showed that tyrosol treatment suppressed the reduction of phospho-tyrosine hydroxylase level in CATH.a cells. Further, the compound repressed MPP+-induced depletion of mitochondrial membrane potential (Δψm) and thereby maintained intracellular ATP production in the cell. The cellular signalling pathway studies revealed that tyrosol protected CATH.a cells from MPP+-induced apoptotic signalling, most likely via activation of PI3K/Akt signalling pathway along with up-regulation of anti-oxidative enzymes (SOD-1 and SOD-2) and DJ-1 protein in the cell. Collectively, present study demonstrates that tyrosol significantly protects dopaminergic neurons from MPP+-induced degradation, and reveals potential neuroprotective mechanism of tyrosol.