Ferulic acid prevents the injury-induced decrease of gamma-enolase expression in brain tissue and HT22 cells.
- Author:
Sang A GIM
1
;
Phil Ok KOH
Author Information
- Publication Type:Original Article
- Keywords: gamma-enolase; ferulic acid; neuroprotection
- MeSH: Adult; Animals; Blotting, Western; Brain Injuries; Brain Ischemia; Brain*; Cell Death; Cell Line; Cerebral Cortex; Glutamic Acid; Humans; Infarction, Middle Cerebral Artery; Male; Neurons; Neuroprotective Agents; Phosphopyruvate Hydratase*; Polymerase Chain Reaction; Proteomics; Rats
- From:Laboratory Animal Research 2014;30(1):8-13
- CountryRepublic of Korea
- Language:English
- Abstract: Ferulic acid is known to act as a protective agent in cerebral ischemia through its anti-oxidant activity. gamma-Enolase is a neuron-specific enolase that also exerts a neuroprotective effect. Here, we investigated whether ferulic acid regulates the expression level of gamma-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 gamma-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 gamma-enolase. Furthermore, in hippocampal-derived cell lines, glutamate exposure also decreased gamma-enolase expression and ferulic acid treatment attenuated this glutamate-induced decrease in gamma-enolase. These findings suggest that ferulic acid mediates a neuroprotective effect by attenuating injury-induced decreases of gamma-enolase expression in neuronal cells.
