Ferulic acid attenuates the cerebral ischemic injury-induced decrease in peroxiredoxin-2 and thioredoxin expression

• Published in: Neuroscience letters Vol. 566; pp. 88 - 92
• Main Authors: Sung, Jin-Hee, Gim, Sang-Ah, Koh, Phil-Ok
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 30.04.2014
• Subjects: Animals; Brain Ischemia - etiology; Brain Ischemia - metabolism; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Coumaric Acids - pharmacology; Ferulic acid; Infarction, Middle Cerebral Artery - complications; Male; Neuroprotection; Neuroprotective Agents - pharmacology; Peroxiredoxin-2; Peroxiredoxins - metabolism; Proteome - metabolism; Rats, Sprague-Dawley; Thioredoxin; Thioredoxins - metabolism; Neuroprotection; Peroxiredoxin-2; Thioredoxin; Ferulic acid
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2014.02.040

•Ferulic acid protects brain tissues against cerebral ischemic injury.•Ferulic acid prevents brain injury-induced decrease of peroxiredoxin-2.•Ferulic acid prevents brain injury-induced decrease of thioredoxin.•Ferulic acid prevents brain injury-induced decrease in the interaction between thioredoxin and ASK1. Ferulic acid, a phenolic phytochemical compound found in various plants, has a neuroprotective effect through its anti-oxidant and anti-inflammation functions. Peroxiredoxin-2 and thioredoxin play a potent neuroprotective function against oxidative stress. We investigated whether ferulic acid regulates peroxiredoxin-2 and thioredoxin levels in cerebral ischemia. Sprague-Dawley rats (male, 210–230g) were treated with vehicle or ferulic acid (100mg/kg) after middle cerebral artery occlusion (MCAO), and cerebral cortex tissues were collected 24h after MCAO. Decreases in peroxiredoxin-2 and thioredoxin levels were elucidated in MCAO-operated animals using a proteomics approach. We found that ferulic acid treatment prevented the MCAO-induced decrease in the expression of peroxiredoxin-2 and thioredoxin. RT-PCR and Western blot analyses confirmed that ferulic acid treatment attenuated the MCAO-induced decrease in peroxiredoxin-2 and thioredoxin levels. Moreover, immunoprecipitation analysis showed that the interaction between thioredoxin and apoptosis signal-regulating kinase 1 (ASK1) decreased during MCAO, whereas ferulic acid prevented the MCAO-induced decrease in this interaction. Our findings suggest that ferulic acid plays a neuroprotective role by attenuating injury-induced decreases in peroxiredoxin-2 and thioredoxin levels in neuronal cell injury.