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.

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Ginkgo biloba extract (EGb 761) exerts a neuroprotective effect against ischemic brain injury through an anti-apoptotic mechanism. Parvalbumin is a calcium buffering protein that plays an important role in modulating intracellular calcium concentration and regulating apoptotic cell death. The aim of this study was to investigate whether EGb 761 affects parvalbumin expression in cerebral ischemic injury. Adult male Sprague-Dawley rats were treated with vehicle or EGb 761 (100 mg/kg) prior to middle cerebral artery occlusion (MCAO) and cerebral cortex tissues were collected 24 h after MCAO. A proteomic approach revealed a reduction in parvalbumin expression in the vehicle-treated animals, whereas EGb 761 pretreatment attenuates the ischemic injury-induced decrease in parvalbumin expression. RT-PCR and Western blot analyses clearly confirmed the fact that EGb 761 prevents the injury-induced decrease in parvalbumin. Moreover, the results of immunohistochemical staining showed that the number of parvalbumin-positive cells was lower in vehicle-treated animals than in sham-operated animals, and EGb 761 averted this decrease. Thus, these results suggest that the maintenance of parvalbumin expression is associated with the neuroprotective function of EGb 761 against neuronal damage induced by ischemia.

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Testicular torsion is a urological emergency that leads to serious testicular damage and male infertility. We performed this study to identify specific proteins that are differentially expressed in response to testicular torsion and detorsion-induced ischemia-reperfusion (I-R) injury. Adult male rats were divided into two groups: a sham-operated group and a testicular I-R group. Testicular torsion was induced by rotating the left testis 720° in a clockwise direction for 1 hr, and then, detorsion was performed for 24 hr. After this testicular tissues were collected, protein analysis was performed using two-dimensional gel electrophoresis and Western blot analyses. Testicular I-R injury resulted in serious histopathologic damage to the germinal cells in the seminiferous tubules and increased the number of TUNEL-positive cells in testicular tissue. Specific protein spots with a greater than 2.5-fold change in intensity between the sham-operated and testicular I-R groups were identified by mass spectrometry. Among these proteins, levels of peroxiredoxin 6, thioredoxin, heterogeneous nuclear ribonucleoproteins, ubiquitin carboxyl terminal hydrolase isozyme L5 and zinc finger AN1-type domain 3 were decreased in the testicular I-R group compared to the sham-operated group. Moreover, Western blot analysis clearly showed the decrease of these proteins in the testicular I-R group. These proteins have spermatogenesis and anti-oxidative functions. These findings suggest that testicular I-R results in cell death due to altered expression of several proteins with spermatogenesis and anti-oxidation functions.