p-Coumaric acid protects against D-galactose induced neurotoxicity by attenuating neuroinflammation and apoptosis in mice brain.

D-galactose (D-gal) induced senescence in rodents is a widely used model for assessment of molecules affecting brain ageing. Chronic administration of D-gal causes neuroinflammation leading to cognitive deficit and memory impairment which represent Alzheimer's dementia. In present study, we investigated the neuroprotective effects of the natural phenol, p-Coumaric acid (PCA) and its underlying mechanism in the chronic D-gal treated mice.

p-Coumaric acid mitigates lipopolysaccharide induced brain damage via alleviating oxidative stress, inflammation and apoptosis.

Objectives: Systemic administration of lipopolysaccharide induces neuroinflammation leading to cognitive deficit and memory impairment. Herein, we investigated the effects of p-Coumaric acid (PCA) in LPS induced neuroinflammation in mice. PCA is reported to possess free radicle scavenging and neuroprotective action.