Ferulic acid prevents the injury-induced decrease of γ-enolase expression in brain tissue and HT22 cells

Ferulic acid is known to act as a protective agent in cerebral ischemia through its anti-oxidant activity. γ-Enolase is a neuron-specific enolase that also exerts a neuroprotective effect. Here, we investigated whether ferulic acid regulates the expression level of γ-enolase in middle cerebral artery occlusion (MCAO)-induced brain injury and glutamate exposure-induced neuronal cell death. Adult male rats were treated with either vehicle or ferulic acid (100 mg/kg, i.v.) after MCAO and cerebral cortex tissues were collected 24 h after MCAO. Using a proteomics approach, we found that γ-enolase expression was decreased in MCAO-injured animals treated with vehicle alone, whereas ferulic acid treatment attenuated this decrease. Reverse-transcription PCR and Western blot analyses confirmed that ferulic acid treatment prevented MCAO injury-induced decrease in γ-enolase. Furthermore, in hippocampal-derived cell lines, glutamate exposure also decreased γ-enolase expression and ferulic acid treatment attenuated this glutamate-induced decrease in γ-enolase. These findings suggest that ferulic acid mediates a neuroprotective effect by attenuating injury-induced decreases of γ-enolase expression in neuronal cells.