animals and treatment : adult male sprague  dawley rats ( 225250 g , 
 n=36 ) were purchased from samtako animal breeding center ( osan , korea ) 
 and were randomly divided into a sham - operated group , vehicle - treated group and 
 resveratrol - treated group ( n=12 per group ) . all procedures for animal use 
 were approved by the institutional animal care and use committee of gyeongsang national 
 university ( gnu-130723-r0050 ) . experimental animals were housed at 1822c under a 12 hr 
 light/12 hr dark cycle and had free access to a pellet diet and tap water . louis , mo , u.s.a . ) was dissolved in 2% dimethyl sulfoxide ( dmso ) as 
 vehicle and was injected intraperitoneally as described previously . resveratrol or vehicle was 
 injected immediately after middle cerebral artery occlusion ( mcao ) . middle cerebral artery occlusion : rats were anesthetized with sodium 
 pentobarbital ( 100 mg / kg ) , and mcao was carried out as described previously . briefly , the right common 
 carotid artery , external carotid and internal carotid were exposed through a midline cut . a 
 4/0 nylon filament with a heated rounded tip was inserted from the external carotid artery 
 into the internal carotid artery and advanced until the rounded tip occluded the origin of 
 the middle cerebral artery . sham - operated animals were subjected to the same procedure , 
 except for insertion of the filament . at 24 hr after the onset of permanent occlusion , 
 animals were decapitated , and the right cerebral cortex was isolated . 2-dimensional gel electrophoresis : proteomic analysis was carried out as 
 our previously described method . 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 . immobilized ph gradients ( ipg , ph 47 and ph 69 , 
 17 cm , bio - rad ) were incubated in rehydration buffer ( 8 m urea , 2% chaps , 20 mm dtt , 0.5% 
 ipg buffer and bromophenol blue ) for 13 hr at room temperature . assayed protein samples were 
 loaded on ipg strips ( ph 47 and 69 ) , and isoelectric focusing ( ief ) was performed as 
 follows : 200 v ( 1 hr ) , 500 v ( 1 hr ) , 1,000 v to 8,000 v ( 30 min ) and 8,000 v ( 5 hr ) using an 
 ipg phore unit ( ge healthcare , uppsala , sweden ) . strips were incubated with equilibration 
 buffer ( 6 m urea , 30% glycerol , 2% sodium dodecyl sulfate , 50 mm tris - hcl and bromophenol 
 blue ) and loaded on gradient gels ( 7.517.5% ) , followed by second - dimension electrophoresis 
 using protein - ii xi electrophoresis equipment ( bio - rad ) . settings were 5 ma per gel for 2 hr 
 followed by 10 ma per gel at 10c . silver staining , image analysis and protein identification : silver 
 staining was performed as follows : fixation ( 12% acetic acid and 50% methanol ) for 2 hr , 
 washing with 50% ethanol and then treatment with 0.2% sodium thiosulfate . gels were washed 
 with deionized water and stained in silver solution ( 0.2% silver nitrate ) . gels were 
 developed in 0.2% sodium carbonate solution , and gel images were collected using an agfar 
 arcus 1200 scanner ( agfar - gevaert , mortsel , belgium ) . pdquest 2-d analysis software 
 ( bio - rad ) was used to analyze differences in protein spots among the different groups . gel particles were 
 digested in trypsin - containing buffer , and the extracted peptides were analyzed using a 
 voyager - detm str biospectrometry workstation ( applied biosystem , forster city , ca , u.s.a . ) 
 for peptide mass fingerprinting . western blot analysis : western blot analysis was carried out as our 
 previously described method [ 13 , 
 32 ] . right cerebral cortex was dissolved in lysis 
 buffer ( 1 m tris  hcl , 5 m sodium chloride , 0.5% sodium deoxycholate , 10% sodium dodecyl 
 sulfate , 1% sodium azide and 10% np-40 ) . protein concentration was determined using a 
 bicinchoninic acid ( bca ) kit ( pierce , rockford , il , u.s.a . ) according to the manufacturer s 
 protocol . equal volumes of protein ( 30 g per sample ) were electrophoresed 
 on 10% sds - page gels , and the proteins were transferred to poly - vinylidene fluoride ( pvdf ) 
 membranes ( millipore , billerica , ma , u.s.a . ) . to minimize nonspecific binding , pvdf membranes were washed in 
 tris - buffered saline containing 0.1% tween-20 ( tbst ) and then incubated with antibodies 
 against the following proteins : peroxiredoxin-5 , isocitrate dehydrogenase [ nad ] , 
 apolipoprotein a - i , ubiquitin carboxy terminal hydrolase l1 , collapsing response mediator 
 protein 2 and actin ( diluted 1:1,000 , cell signaling technology , beverly , ma , u.s.a . ) . ecl western 
 blot analysis system ( amersham pharmacia biotech , piscataway , nj , u.s.a . ) was used for 
 detection according to the manufacturer s protocol . the intensity analysis was carried out 
 using sigmagel 1.0 ( jandel scientific , san rafael , ca , u.s.a . ) and sigmaplot 4.0 ( spss inc . , reverse transverse - pcr amplification : total rna from right cerebral 
 cortices was extracted using trizol reagent ( invitrogen , carlsbad , ca , u.s.a . ) following the 
 manufacturer s protocol . for reverse transcription , we used superscript iii reverse 
 transcriptase from invitrogen following the manufacturer s manuals . the primer sequences are 
 represented in table 1table 1.sequence of the primers used for pcr amplificationgeneprimer sequences ( f , forward ; r , reverse)product size ( bp)peroxiredoxin-5f:5-ggagtccctggggcatttac-3392r:5-gacattctggtcagggcctc-3nad ( + ) -dependent isocitrate 
 dehydrogenasef:5-aaaaatccatggcggttctgtg-3404r:5-ggtccccataggcgtgtcg-3apolipoprotein a - if:5-tgttggtcgcctacaggaac-3223r:5- tcgcgtttttgtgaagctcg-3ubiquitin carboxyl terminal hydrolase 
 isozyme l1 ( uch - l1)f:5-ctagggctggaggaggagac-3296r:5-ttgtcccctgaagagagagc-3collapsing response mediator protein 2 
 ( crmp-2)f:5-tggtttcagcttgtctggtg-3454r:5 -tgacaggaaggtgctgactg-3-actinf:5-gggtcagaaggactcctacg-3238r:5- tttcactgcggctgatgtag-3. the amplification pcr reaction consisted of an initial denaturation at 94c 
 for 5 min , followed by 35 cycles from 94c for 30 sec , annealing at 54c for 30 sec and an 
 extension at 72c for 1 min and a final extension for 10 min at 72c . rt - pcr products were 
 separated on a 1% agarose gel and visualized under uv light . the intensity analysis of 
 rt - pcr products was carried out using sigmagel 1.0 ( jandel scientific ) and sigmaplot 4.0 
 ( spss inc . ) . data analysis : all data are expressed as means  sem . the results for each 
 group were compared by one - way analysis of variance ( anova ) followed by student s 
 t - test . two - dimensional electrophoresis ( 2-de ) maps were generated for cerebral cortex protein 
 spots from sham - operated , vehicle - treated and resveratrol - treated animals ( ph range 47 and 
 ph 69 ) . approximately 980 protein spots per image were observed . we detected thirty - four 
 protein spots with more than a 2.5-fold change in intensity . among these protein spots , twenty - nine proteins were clearly identified by maldi - tof analysis with a protein sequence 
 coverage ranging from 2167% ( fig . 1.two-dimensional sds - page analysis of proteins in the cerebral cortex from 
 sham - operated ( a and b ) , vehicle - treated ( c and d ) and resveratrol - treated ( e and f ) 
 animals after middle cerebral artery occlusion ( mcao ) . isoelectric focusing was 
 performed at ph 47 and ph 69 using ipg strips , followed by second - dimensional 
 separation on 7.517.5% gradient sds gels stained with silver . squares indicate the 
 protein spots that were differentially expressed between vehicle- and 
 resveratrol - treated groups . , table 2table 2.list of identified proteins that were significantly differentially expressed in 
 vehicle- and resveratrol - treated animalsspotno.protein nameaccessionno.mw(kda)pimassmatchedsequencecoverage ( % ) ratio veh /shamratio res / sham160 kda heat shock proteinp6303960.915.9111/13332%3.01  0.13 * 1.15  0.12 * 2collapsing response mediator protein 2p4794283.856.647/10929%3.03  0.14 * 1.10  0.13 * 3collapsing response mediator protein 2p4794262.276.024/10352%2.78  0.12 * 1.09  0.12 * 4rab , gtpase - gdp dissociation stimulation stimulator 
 1p5230666.405.220/15653%0.32  0.04 * 1.02  0.07 * 5unknown2.93  0.12 * 1.08  0.02 * 6unknown0.33  0.03 * 0.97  0.02 * 7eukaryotic initiation factor 4a - iiq5rki146.735.3316/8240%0.36  0.04 * 0.89  0.05 * 8succinyl - coa ligase subunit betaq9z2i950.277.7511/7424%0.34  0.03 * 1.01  0.03 * 9adenosine kinaseq6464040.105.7212/9541%0.33  0.02 * 1.02  0.02 * 10map kinase kinase 1q0198643.436.1812/7230%0.35  0.03 * 0.98  0.03 * 11adenosylhomocysteinasep1076047.506.0715/13233%0.31  0.03 * 1.01  0.04 * 12protein phosphatase 2a , subunit bp5838936.595.889/5629%0.32  0.02 * 0.89  0.02 * 13isocitrate dehydrogenase[nad+ ] subunit alphaq99na539.586.478/9331%0.31  0.04 * 0.87  0.02 * 14-enolasep0732347.145.0014/7035%0.27  0.03 * 0.91  0.02 * 15ubiquitin carboxy - terminal hydrolase l1q7tqi331.254.8511/6650%0.30  0.03 * 1.02  0.02 * 16thioredoxcinq920j432.234.848/8742%0.22  0.03 * 0.89  0.04 * 17mu - crystallinq9qyu433.535.349/8624%0.15  0.02 * 0.94  0.02 * 18hippocalcinp6274922.325.310/10252%0.25  0.03 * 0.96  0.02 * 19proteasome subunit alpha type3p1842228.405.37/11227%0.20  0.03 * 0.97  0.02 * 20apolipoprotein a - ip04463930.045.5216/11650%0.34  0.02 * 1.05  0.03 * 21pyruvate kinase isoenzyme m1/m2p1198057.826.6319/8042%2.51  0.03 * 1.08  0.03 * 22pyruvate kinase isoenzyme m1/m2p1198057.826.6319/8042%2.73  0.03 * 1.13  0.04 * 23unknown0.27  0.03 * 1.05  0.03 * 24mitogen - activated protein ( map ) kinase 1p6308641.276.510/9636%0.29  0.03 * 0.97  0.02 * 25alcohol dehydrogenase ( nadp+)p5163536.506.89/10428%0.33  0.03 * 1.02  0.03 * 26unknown0.32  0.03 * 0.99  0.02 * 27obg - like atpase 1a0jpj744.507.626/6821%0.33  0.02 * 1.02  0.03 * 28malate dehydrogenasep0463635.688.923/8067%0.17  0.04 * 1.07  0.02 * 29malate dehydrogenasep0463635.688.923/8067%0.32  0.04 * 0.99  0.03 * 30nucleoside diphosphate kinase bp1980417.286.98/8649%0.33  0.02 * 0.95  0.03 * 31peroxiredoxin-5q9r06322.178.99/11446%0.24  0.03 * 0.97  0.02 * 32cb1 cannabinoid receptor - interacting protein 1q5m7a718.647.75/12031%0.31  0.03 * 0.95  0.03 * 33adenylate kinase isoenzyme1p3906921.587.712/9534%0.34  0.03 * 0.87  0.02 * 34unknown0.15  0.04 * 0.79  0.03*protein names and accession numbers are listed according to the swiss - prot database . mw , molecular weight ; pi , isoelectric point . ratio is described as spots intensity of 
 mcao - operated to spots intensity of sham - operated . however , five proteins were not identified by maldi - tof analysis and named 
 as unknown proteins . among these identified proteins , we focused on peroxiredoxin-5 , 
 isocitrate dehydrogenase [ nad ] , apolipoprotein a - i , ubiquitin carboxy terminal 
 hydrolase l1 ( uch - l1 ) and collapsing response mediator protein 2 ( crmp-2 ) ( fig . 2fig . magnified pictures of 
 peroxiredoxin-5 , isocitrate dehydrogenase [ nad ] , apolipoprotein a - i , 
 ubiquitin carboxy terminal hydrolase l1 ( uch - l1 ) and collapsing response mediator 
 protein 2 ( crmp-2 ) protein spots in the cerebral cortex from sham - operated , 
 vehicle - treated and resveratrol - treated animals after middle cerebral artery occlusion 
 ( mcao ) . two - dimensional sds - page analysis of proteins in the cerebral cortex from 
 sham - operated ( a and b ) , vehicle - treated ( c and d ) and resveratrol - treated ( e and f ) 
 animals after middle cerebral artery occlusion ( mcao ) . isoelectric focusing was 
 performed at ph 47 and ph 69 using ipg strips , followed by second - dimensional 
 separation on 7.517.5% gradient sds gels stained with silver . squares indicate the 
 protein spots that were differentially expressed between vehicle- and 
 resveratrol - treated groups . protein names and accession numbers are listed according to the swiss - prot database . ratio is described as spots intensity of 
 mcao - operated to spots intensity of sham - operated . magnified pictures of 
 peroxiredoxin-5 , isocitrate dehydrogenase [ nad ] , apolipoprotein a - i , 
 ubiquitin carboxy terminal hydrolase l1 ( uch - l1 ) and collapsing response mediator 
 protein 2 ( crmp-2 ) protein spots in the cerebral cortex from sham - operated , 
 vehicle - treated and resveratrol - treated animals after middle cerebral artery occlusion 
 ( mcao ) . western blot analysis showed that peroxiredoxin-5 , isocitrate dehydrogenase 
 [ nad ] , apolipoprotein a - i and uch - l1 levels decreased in vehicle - treated 
 animals , whereas resveratrol treatment prevented the injury - induced decrease in expression 
 of these proteins . protein expression levels are represented as the ratio of intensity of 
 the protein to that of actin . peroxiredoxin-5 levels were lower in vehicle - treated animals 
 than resveratrol- and sham - operated animals , and these proteins were expressed at similar 
 levels in the latter two groups ( fig . 3fig . 3.western blot analysis of peroxiredoxin-5 ( prx-5 ) , isocitrate dehydrogenase 
 [ nad ] ( icdh ) , apolipoprotein a - i ( apoa - i ) , ubiquitin carboxy terminal 
 hydrolase l1 ( uch - l1 ) and collapsing response mediator protein 2 ( crmp-2 ) in the 
 cerebral cortex from sham - operated , vehicle - treated and resveratrol - treated animals 
 after middle cerebral artery occlusion ( mcao ) . peroxiredoxin-5 levels were 0.57  0.04 and 0.79  0.03 in vehicle- and 
 resveratrol - treated animals . isocitrate dehydrogenase [ nad ] levels were 0.42  
 0.03 and 0.67  0.03 in vehicle- and resveratrol - treated animals . apolipoprotein a - i levels 
 were 0.47  0.03 and 0.65  0.02 in vehicle- and resveratrol - treated animals , respectively . uch - l1 levels were 0.48  0.02 and 0.76  0.03 in vehicle- and resveratrol - treated animals , 
 respectively ( fig . 3 ) . in contrast , crmp-2 
 expression increased in vehicle - treated animals relative to resveratrol - treated animals and 
 sham - operated animals . crmp-2 levels were 1.07  0.02 and 0.85  0.03 in vehicle- and 
 resveratrol - treated animals , respectively ( fig . moreover , rt - pcr analysis clearly demonstrated that peroxiredoxin-5 , isocitrate 
 dehydrogenase [ nad ] , apolipoprotein a - i and uch - l1 levels decreased in 
 vehicle - treated animals , whereas resveratrol treatment attenuated the injury - induced 
 decreases in these mrna levels . however , crmp-2 mrna increased in vehicle - treated animals , 
 whereas resveratrol treatment attenuated this increase ( fig . 4.representative photos of rt - pcr analysis of peroxiredoxin-5 ( prx-5 ) , isocitrate 
 dehydrogenase [ nad ] ( icdh ) , apolipoprotein a - i ( apoa - i ) , ubiquitin carboxy 
 terminal hydrolase l1 ( uch - l1 ) and collapsing response mediator protein 2 ( crmp-2 ) in 
 the cerebral cortex from sham - operated , vehicle - treated and resveratrol - treated 
 animals after middle cerebral artery occlusion ( mcao ) . the band intensity of rt - pcr product was normalized to 
 that of actin product . the intensity of rt - pcr product was normalized to that of actin product . peroxiredoxin-5 levels were 0.36  0.02 and 0.73  0.02 in vehicle- and resveratrol - treated 
 animals . isocitrate dehydrogenase [ nad ] levels were 0.35  0.02 and 0.78  0.03 
 in vehicle- and resveratrol - treated animals . apolipoprotein a - i levels were 0.24  0.02 and 
 0.82  0.02 in vehicle- and resveratrol - treated animals , respectively . uch - l1 levels were 
 0.38  0.02 and 0.83  0.03 in vehicle- and resveratrol - treated animals , respectively ( fig . crmp-2 levels were 0.94  0.02 and 0.41  
 0.02 in vehicle- and resveratrol - treated animals , respectively ( fig . western blot analysis of peroxiredoxin-5 ( prx-5 ) , isocitrate dehydrogenase 
 [ nad ] ( icdh ) , apolipoprotein a - i ( apoa - i ) , ubiquitin carboxy terminal 
 hydrolase l1 ( uch - l1 ) and collapsing response mediator protein 2 ( crmp-2 ) in the 
 cerebral cortex from sham - operated , vehicle - treated and resveratrol - treated animals 
 after middle cerebral artery occlusion ( mcao ) . representative photos of rt - pcr analysis of peroxiredoxin-5 ( prx-5 ) , isocitrate 
 dehydrogenase [ nad ] ( icdh ) , apolipoprotein a - i ( apoa - i ) , ubiquitin carboxy 
 terminal hydrolase l1 ( uch - l1 ) and collapsing response mediator protein 2 ( crmp-2 ) in 
 the cerebral cortex from sham - operated , vehicle - treated and resveratrol - treated 
 animals after middle cerebral artery occlusion ( mcao ) . the band intensity of rt - pcr product was normalized to 
 that of actin product . we previously reported that ferulic acid exerts a neuroprotective effect against mcao 
 injury by modulating several proteins . such as resveratrol , ferulic 
 acid is a phenolic compound that extracted from plant . ferulic acid and resveratrol have 
 similar functions , including anti - inflammatory and anti - oxidative effects . we 
 identified differentially expressed proteins following resveratrol treatment in focal 
 cerebral ischemia . among these identified proteins peroxiredoxins are thioredoxin peroxidases that participate the elimination of hydrogen 
 peroxide and neutralize other reactive oxygen species ( ros ) . moreover , peroxiredoxins 
 peroxidases are anti - oxidant proteins that preserve the integrity of the cell against 
 oxidative stress . , peroxiredoxin-5 has a broader activity against 
 both ros and reactive nitrogen species compared with other isoforms of peroxiredoxins 
 . ischemic stroke leads to the 
 generation of free radicals , and this excessive production of free radicals disrupts the 
 hemostatic environment and triggers neuronal cells death . we found that peroxiredoxin-5 
 expression decreases in ischemic brain injury , whereas resveratrol attenuates the 
 injury - induced decline in this protein . our results demonstrate that 
 resveratrol minimizes the decrease of peroxiredoxin-5 in focal cerebral ischemia . nad ( + ) -dependent isocitrate dehydrogenase is located in the mitochondria and is associated 
 with energy metabolism and mitochondrial function . nad ( + ) -dependent isocitrate 
 dehydrogenase plays a pivotal role in the production of nadh from nad+ in the krebs cycle . nadh regulates various biological functions , including energy metabolism and anti - oxidation 
 activity . however , oxidative 
 stress causes a decrease in the concentration of nad+ and cessation of energy metabolism 
 . resveratrol protects the brain 
 by up - regulating mitochondrial superoxide dismutase , which reduces oxidative stress and 
 decreases cell death . moreover , resveratrol increases the activities of adenylate kinase and isocitrate 
 dehydrogenase in heart ischemia . we demonstrated that ischemic brain injury results in a decrease in the expression of 
 isocitrate dehydrogenase [ nad ] using a proteomics approach . rt - pcr and western 
 blot analyses clearly confirmed that resveratrol prevents the injury - induced decrease in 
 isocitrate dehydrogenase [ nad ] expression caused by mcao . these results suggest that 
 maintenance of isocitrate dehydrogenase levels by resveratrol not only has a positive effect 
 on energy metabolism , but is also neuroprotective effect . apolipoprotein a - i is an essential constituent of high density lipoprotein and is a key 
 player in the transport and delivery of lipids . it has anti - oxidant and anti - inflammatory properties and modifies 
 various immune functions . our proteomics approach revealed 
 that apolipoprotein a - i levels decreases in response to focal cerebral ischemia . these 
 results are consistent with the decreases in apolipoprotein a - i levels in neurodegenerative 
 diseases . resveratrol treatment attenuates the mcao - induced decrease in apolipoprotein a - i 
 expression . a previous study demonstrated that resveratrol treatment increases expression of 
 apolipoprotein a - i and inhibits the lipid peroxidation . together , these findings suggest 
 that maintenance of apolipoprotein a - i expression by resveratrol contributes to attenuation 
 of cell damage in cerebral ischemia . ubiquitin carboxy terminal hydrolase l1 ( uch - l1 ) is a neuron specific de - ubiquitinating 
 enzyme , because it is exclusive expressed in brain tissue . uch - l1 ubiquitinates damaged 
 proteins , such as oxidized proteins and aggregated proteins , for degradation by the 
 proteasome system . thus , uch - l1 plays 
 an essential role in the maintenance of cell homeostasis . uch - l1 prevents neuronal cell 
 death from oxidative stress , and down - regulation of uch - l1 leads to neuronal degeneration 
 [ 1 , 24 ] . moreover , it has been reported that down - regulation of uch - l1 is associated 
 with parkinson s disease and alzheimer s disease . our proteomics data revealed that 
 uch - l1 levels decreased in response to cerebral ischemia , whereas resveratrol treatment 
 attenuated this decrease in expression . we confirmed these results using rt - pcr and western 
 blot analyses . a decrease in uch - l1 expression would lead to an imbalance between 
 ubiquitination and de - ubiquitination and accumulation of aggregated and compromised protein , 
 thereby inducing cell death . our results demonstrate that resveratrol prevents the down - regulation of uch - l1 in focal 
 cerebral ischemia . we can make an inference from these results that regulation of uch - l1 by 
 resveratrol maintains the cell homeostasis and preserves neuronal cells against mcao . collapsing response mediator protein 2 ( crmp-2 ) regulates various neuronal activities 
 including neuronal maturation , regeneration and axonal growth [ 6 , 27 ] . crmp-2 is involved in pathological disorders of neurons and is increased by 
 ischemic brain injury . this is consistent with 
 previous studies that crmp-2 is up - regulated after focal cerebral ischemia . these 
 results suggest that the regulation of crmp-2 expression by resveratrol contributes to the 
 neuroprotective effect of resveratrol . in conclusion , we provide evidence that resveratrol 
 modulates the expression of various specific proteins in focal cerebral ischemia . specifically , resveratrol attenuates the injury - induced decrease in expression of 
 peroxiredoxin-5 , isocitrate dehydrogenase [ nad ] , apolipoprotein a - i and uch - l1 . however , resveratrol prevents an increase in expression of crmp-2 in response to 
 mcao - induced injury . isocitrate dehydrogenase 
 [ nad ] , apolipoprotein a - i and ubiquitin carboxy terminal hydrolase l1 are 
 known to have neuroprotective effects . the results of this study show that resveratrol prevents the injury - induced 
 decrease of peroxiredoxin-5 , isocitrate dehydrogenase [ nad ] , apolipoprotein a - i 
 and ubiquitin carboxy terminal hydrolase l1 levels and these proteins are involved in 
 oxidative stress and energy metabolism . in conclusion , these results provide evidence that 
 resveratrol regulates expression of various proteins that associated with oxidative stress 
 and energy metabolism in focal cerebral ischemia .
abstractresveratrol 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 .