Identification of Proteins Regulated by Ferulic Acid in a Middle Cerebral Artery Occlusion Animal Model-A Proteomics Approachopen access
- Authors
- Sung, Jin-Hee; Cho, Eun-Hae; Cho, Jae-Hyeon; Won, Chung-Kil; Kim, Myeong-Ok; Koh, Phil-Ok
- Issue Date
- Nov-2012
- Publisher
- JAPAN SOC VET SCI
- Keywords
- ferulic acid; ischemia; proteomics
- Citation
- JOURNAL OF VETERINARY MEDICAL SCIENCE, v.74, no.11, pp 1401 - 1407
- Pages
- 7
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- JOURNAL OF VETERINARY MEDICAL SCIENCE
- Volume
- 74
- Number
- 11
- Start Page
- 1401
- End Page
- 1407
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/21945
- DOI
- 10.1292/jvms.12-0063
- ISSN
- 0916-7250
- Abstract
- Ferulic acid plays a neuroprotective role in cerebral ischemia. The aim of this study was to identify the proteins that are differentially expressed following ferulic acid treatment during ischemic brain injury using a proteomics technique. Middle cerebral artery occlusion (MCAO) was performed to induce a focal cerebral ischemic injury in adult male rats, and ferulic acid (100 mg/kg) or vehicle was administered immediately after MCAO. Brain tissues were collected 24 hr after MCAO. The proteins in the cerebral cortex were separated using two-dimensional gel electrophoresis and were identified by mass spectrometry. We detected differentially expressed proteins between vehicle- and ferulic acid-treated animals. Adenosylhomocysteinase, isocitrate dehydrogenase [NAD(+)], mitogen-activated protein kinase kinase 1 and glyceraldehyde-3-phosphate dehydrogenase were decreased in the vehicle-treated group, and ferulic acid prevented the injury-induced decreases in these proteins. However, pyridoxal phosphate phosphatase and heat shock protein 60 were increased in the vehicle-treated group, while ferulic acid prevented the injury-induced increase in these proteins. It is accepted that these enzymes are involved in cellular metabolism and differentiation. Thus, these findings suggest evidence that ferulic acid plays a neuroprotective role against focal cerebral ischemia through the up- and down-modulation of specific enzymes.
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