Sang-Ah Gim
Gyeongsang National University
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Featured researches published by Sang-Ah Gim.
Neuroscience Letters | 2014
Jin-Hee Sung; Sang-Ah Gim; Phil-Ok Koh
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, 210-230g) were treated with vehicle or ferulic acid (100mg/kg) after middle cerebral artery occlusion (MCAO), and cerebral cortex tissues were collected 24h 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.
Laboratory Animal Research | 2012
Jin-Hee Sung; Fawad-Ali Shah; Eun-Hae Cho; Sang-Ah Gim; Seong-Jun Jeon; Kyung Min Kim; Young Min Kim; Myeong-Ok Kim; Phil-Ok Koh
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.
Journal of Surgical Research | 2015
Sang-Ah Gim; Phil-Ok Koh
BACKGROUND Melatonin exerts a protective effect during hepatic ischemia-reperfusion (I/R) injury through modulation of the apoptotic cell death program. Mitogen-activated protein kinases mediate various intracellular processes such as cell differentiation, survival, and death. This study investigated whether melatonin exerts a protective effect through the activation of Raf-MEK-ERK and its downstream targets, including 90 ribosomal S6 kinase (p90RSK) and Bad, during hepatic I/R damage. METHODS Hepatic ischemia was induced in mice by occlusion of the hepatic artery, portal vein, and bile duct. Adult mice were subjected to 1 h of hepatic ischemia and 3 h of reperfusion. Vehicle or melatonin (10 mg/kg, intraperitoneal) was injected 15 min before ischemia and just before reperfusion. Serum aspartate aminotransferase and alanine aminotransferase levels were measured, and terminal deoxynucleotidyl transferase dUTP nick-end labeling histochemistry was performed. Moreover, Western blot and immunoprecipitation analyses were performed. RESULTS Melatonin treatment attenuated hepatic I/R-induced increases in alanine aminotransferase and aspartate aminotransferase levels and also ameliorated hepatic injury-induced pathologic lesions and increases of positive terminal deoxynucleotidyl transferase dUTP nick-end labeling staining in hepatic tissues. Hepatic I/R injury induced decreases in the phosphorylation of Raf-1, MEK1/2, and extracellular-regulated kinase (ERK)1/2, whereas melatonin attenuated decreases in these phosphorylation levels. Moreover, melatonin prevented the injury-induced decreases in phosphorylation of downstream targets, p90RSK and Bad. Immunoprecipitation analysis showed that the interaction between phospho-Bad and 14-3-3 was decreased in vehicle-treated animals, while melatonin prevented this decrease. Melatonin also attenuated the injury-induced increase in cleaved caspase-3. In cultured hepatocytes, melatonin treatment prevented the hydrogen peroxide-induced cell death and decrease in phosphorylation of ERK1/2. Moreover, blocking MEK by PD98059 attenuated the effect of melatonin. CONCLUSIONS These data suggest that melatonin protects hepatic cells against hepatic I/R damage through the activation of the Raf-MEK-ERK cascade and phosphorylation of its downstream targets.
Journal of Surgical Research | 2016
Fawad-Ali Shah; Sang-Ah Gim; Jin-Hee Sung; Seong-Jun Jeon; Myeong-Ok Kim; Phil-Ok Koh
BACKGROUND Curcumin is known to have a neuroprotective effect against cerebral ischemia. The objective of this study was to identify various proteins that are differentially expressed by curcumin treatment in focal cerebral ischemia using a proteomic approach. METHODS Adult male rats were treated with vehicle or curcumin 1 h after middle cerebral artery occlusion. Brain tissues were collected 24 h after the onset of middle cerebral artery occlusion, and cerebral cortices proteins were identified by two-dimensional gel electrophoresis and mass spectrometry. RESULTS We detected several proteins with altered expression levels between vehicle- and curcumin-treated animals. Among these proteins, ubiquitin carboxy-terminal hydrolase L1, isocitrate dehydrogenase, adenosylhomocysteinase, and eukaryotic initiation factor 4A were decreased in the vehicle-treated animal, and curcumin treatment attenuated the injury-induced decreases of these proteins. Conversely, pyridoxal phosphate phosphatase was increased in the vehicle-treated animal, and curcumin treatment prevented decreases in this protein. The identified altered proteins are associated with cellular metabolism and differentiation. CONCLUSIONS The results of this study suggest that curcumin exerts a neuroprotective effect by regulating the expression of various proteins in focal cerebral ischemia.
Journal of Veterinary Medical Science | 2014
Fawad-Ali Shah; Sang-Ah Gim; Myeong-Ok Kim; Phil-Ok Koh
ABSTRACT 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.
Journal of Veterinary Medical Science | 2014
In-Ohk Ouh; Min-Goo Seo; Fawad-Ali Shah; Sang-Ah Gim; Phil-Ok Koh
ABSTRACT 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.
Journal of Surgical Research | 2016
Jin-Hee Sung; Fawad-Ali Shah; Sang-Ah Gim; Phil-Ok Koh
Journal of Agriculture and Life Science | 2016
Sang-Ah Gim; Phil-Ok Koh
한국실험동물학회 학술발표대회 논문집 | 2016
Sora Lee; Sang-Ah Gim; Phil-Ok Koh
한국실험동물학회 학술발표대회 논문집 | 2015
Sang-Ah Gim; Dong-Ju Park; Fawad-Ali Shah; Phil-Ok Koh