Ferulic acid attenuates the cerebral ischemic injury-induced decrease in peroxiredoxin-2 and thioredoxin expression
- Authors
- Sung, Jin-Hee; Gim, Sang-Ah; Koh, Phil-Ok
- Issue Date
- 30-Apr-2014
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Ferulic acid; Neuroprotection; Peroxiredoxin-2; Thioredoxin
- Citation
- NEUROSCIENCE LETTERS, v.566, pp 88 - 92
- Pages
- 5
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- NEUROSCIENCE LETTERS
- Volume
- 566
- Start Page
- 88
- End Page
- 92
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/19031
- DOI
- 10.1016/j.neulet.2014.02.040
- ISSN
- 0304-3940
1872-7972
- Abstract
- 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, 210-230 g) were treated with vehicle or ferulic acid (100 mg/kg) after middle cerebral artery occlusion (MCAO), and cerebral cortex tissues were collected 24 h 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. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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