Sodium cinnamate, a naturally occurring low-toxicity aromatic fatty acid with oral activity, exhibits neuroprotective and anti-inflammatory properties.

Sodium cinnamate (0.05, 0.4, 3.2 mM; 6, 12, 24 h) induces apoptosis in HT-144 cells at a concentration of 3.2 mM after 24 hours.

Administration of sodium cinnamic acid (100 mg/kg; gavage) activates Peroxisome Proliferator-Activated Receptor alpha (PPARα), enhances the protection of dopaminergic neurons from degeneration, restores striatal fibers and neurotransmitters, and improves the behavior of mice intoxicated with MPTP. Using a model involving 6-8 week-old C57BL/6 mice treated with 18 mg/kg MPTP-HCl, administered intraperitoneally at 2-hour intervals for four doses, sodium cinnamic acid was started 3 hours after the last MPTP injection. The results indicated protection of nigral TH levels and striatal innervation, restoration of locomotor deficits, increased activation of PPARα in primary mouse astrocytes, and protection of striatal TH mediated by PPARα activation.