Figure 1.

Neuroprotective effects of propionic acid after neuronal damage by rotenone.

Treatment of dopaminergic midbrain neurons with rotenone leads to an inhibition of the mitochondrial respiratory chain and the induction of oxidative stress, resulting in axonal loss and cell death. Propionic acid increases cell survival, neurite outgrowth as well as the gene expression of TH and aSyn. Potential mechanisms of action are via G protein-coupled receptors or modification of histone deacetylase activity. The figure is created with BioRender.com. ATP: Adenosine triphosphate; DAT: dopamine transporter; MAP2: microtubule-associated protein 2; ROS: reactive oxygen species; SYP: synaptophysin; TH: tyrosine hydroxylase.