Identification of Proteins Regulated by Ferulic Acid in a Middle Cerebral Artery Occlusion Animal Model-A Proteomics Approach

Sung, Jin-Hee; Cho, Eun Hae; Cho, Jae‐Hyeon; Won, Chung-Kil; Kim, Myeong-Ok; Koh, Phil-Ok

doi:10.1292/jvms.12-0063

Cited by 10 publications

(18 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We previously demonstrated that ferulic acid contributes to the up- and down-regulation of various specific proteins during MCAO injury. Among these proteins, this study was focused on PP2A subunit B expression [16].…”

Section: Discussionmentioning

confidence: 99%

Ferulic Acid Attenuates the Injury-Induced Decrease of Protein Phosphatase 2A Subunit B in Ischemic Brain Injury

Koh

2013

PLoS ONE

Self Cite

View full text Add to dashboard Cite

BackgroundFerulic acid provides a neuroprotective effect during cerebral ischemia through its anti-oxidant function. Protein phosphatase 2A (PP2A) is a serine and threonine phosphatase that contributes broadly to normal brain function. This study investigated whether ferulic acid regulates PP2A subunit B in a middle cerebral artery occlusion (MCAO) animal model and glutamate toxicity-induced neuronal cell death.Methodology/Principal FindingsMCAO was surgically induced to yield permanent cerebral ischemic injury in rats. The rats were treated with either vehicle or ferulic acid (100 mg/kg, i.v.) immediately after MCAO, and cerebral cortex tissues were collected 24 h after MCAO. A proteomics approach, RT-PCR, and Western blot analyses performed to identification of PP2A subunit B expression levels. Ferulic acid significantly reduced the MCAO-induced infarct volume of the cerebral cortex. A proteomics approach elucidated the reduction of PP2A subunit B in MCAO-induced animals, and ferulic acid treatment prevented the injury-induced reduction in PP2A subunit B levels. RT-PCR and Western blot analyses also showed that ferulic acid treatment attenuates the injury-induced decrease in PP2A subunit B levels. Moreover, the number of PP2A subunit B-positive cells was reduced in MCAO-induced animals, and ferulic acid prevented these decreases. In cultured neuronal cells, ferulic acid treatment protected cells against glutamate toxicity and prevented the glutamate-induced decrease in PP2A subunit B.Conclusions/SignificanceThese results suggest that the maintenance of PP2A subunit B by ferulic acid in ischemic brain injury plays an important role for the neuroprotective function of ferulic acid.

show abstract

Section: Discussionmentioning

confidence: 99%

Ferulic Acid Attenuates the Injury-Induced Decrease of Protein Phosphatase 2A Subunit B in Ischemic Brain Injury

Koh

2013

PLoS ONE

Self Cite

View full text Add to dashboard Cite

show abstract

“…We previously reported that ferulic acid exerts a neuroprotective effect against MCAO injury by modulating several proteins [32]. Such as resveratrol, ferulic acid is a phenolic compound that extracted from plant.…”

Section: Discussionmentioning

confidence: 99%

“…2-Dimensional gel electrophoresis : Proteomic analysis was carried out as our previously described method [32]. Proteins were extracted from the right cerebral cortex by homogenization in buffer solution (8 M urea, 4% CHAPS, ampholytes and 40 mM Tris–HCl) followed by centrifugation at 16,000 g. Protein concentration was determined by the Bradford method (Bio-Rad, Hercules, CA, U.S.A.) according to the manufacturer’s protocol.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Proteomic Identification of Proteins Differentially Expressed in Response to Resveratrol Treatment in Middle Cerebral Artery Occlusion Stroke Model

et al. 2014

Self Cite

View full text Add to dashboard Cite

Resveratrol has a neuroprotective effect against cerebral ischemia. The objective of this study was to identify proteins that are differentially expressed in the cerebral cortex of vehicle- and resveratrol-treated animals during ischemic injury. Focal cerebral ischemia was induced as middle cerebral artery occlusion (MCAO) in male rats. Rats were treated with vehicle or resveratrol before MCAO, and cerebral cortex was collected 24 hr after MCAO. Cerebral cortex proteins were identified by two-dimensional gel electrophoresis and mass spectrometry. Several proteins were identified as differentially expressed between vehicle- and resveratrol-treated animals. Among these proteins, expression of peroxiredoxin-5, isocitrate dehydrogenase [NAD+], apolipoprotein A-I and ubiquitin carboxy terminal hydrolase L1 was decreased in the vehicle-treated group, whereas resveratrol attenuated the injury-induced decrease in expression of these proteins. However, expression of collapsing response mediator protein 2 was increased in the vehicle-treated group, whereas resveratrol prevented the injury-induced increase in the expression of this protein. These findings suggest that resveratrol modulates the expression of various proteins that associated with oxidative stress and energy metabolism in focal cerebral ischemia.

show abstract

“…Moreover, ferulic acid exerts potent protection against glutamate‐induced toxicity (Yu et al, ) and significantly reduces the infarct volume in a cerebral ischemic injury animal model. We previously demonstrated that ferulic acid plays a neuroprotective role against focal cerebral ischemia through the up‐ and down‐modulation of various proteins (Sung et al, in press).…”

Section: Introductionmentioning

confidence: 99%

Ferulic acid prevents cerebral ischemic injury‐induced reduction of hippocalcin expression

Koh

2013

Synapse

Self Cite

View full text Add to dashboard Cite

Intracellular calcium overload is a critical pathophysiological factor in ischemic injury. Hippocalcin is a neuronal calcium sensor protein that buffers intracellular calcium levels and protects cells from apoptotic stimuli. Ferulic acid exerts a neuroprotective effect in cerebral ischemia through its anti-oxidant and anti-inflammation activity. This study investigated whether ferulic acid contributes to hippocalcin expression during cerebral ischemia and glutamate exposure-induced neuronal cell death. Rats were immediately treated with vehicle or ferulic acid (100 mg/kg, i.v.) after middle cerebral artery occlusion (MCAO). Brain tissues were collected 24 h after MCAO and followed by assessment of cerebral infarct. Ferulic acid reduced MCAO-induced infarct regions. A proteomics approach elucidated a decrease in hippocalcin in MCAO-operated animals, ferulic acid attenuates the injury-induced decrease in hippocalcin expression. Reverse transcription-polymerase chain reaction and Western blot analyses confirmed that ferulic acid prevents the injury-induced decrease in hippocalcin. In cultured HT22 hippocampal cells, glutamate exposure increased the intracellular Ca(2+) levels, whereas ferulic acid attenuated this increase. Moreover, ferulic acid attenuated the glutamate toxicity-induced decrease in hippocalcin expression. These findings can suggest the possibility that ferulic acid exerts a neuroprotective effect through modulating hippocalcine expression and regulating intracellular calcium levels.

show abstract

Identification of Proteins Regulated by Ferulic Acid in a Middle Cerebral Artery Occlusion Animal Model-A Proteomics Approach

Cited by 10 publications

References 18 publications

Ferulic Acid Attenuates the Injury-Induced Decrease of Protein Phosphatase 2A Subunit B in Ischemic Brain Injury

Ferulic Acid Attenuates the Injury-Induced Decrease of Protein Phosphatase 2A Subunit B in Ischemic Brain Injury

Proteomic Identification of Proteins Differentially Expressed in Response to Resveratrol Treatment in Middle Cerebral Artery Occlusion Stroke Model

Ferulic acid prevents cerebral ischemic injury‐induced reduction of hippocalcin expression

Contact Info

Product

Resources

About