Publications (34)69.69 Total impact
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Article: Neuroprotective effects of Alpinia katsumadai against experimental ischemic damage via control of oxidative stress.
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ABSTRACT: Context: Alpinia katsumadai (Zingiberaceae) has been identified by the National Plant Quarantine Service in Korea. The extract of Alpinia katsumadai seed (EAKS) has antioxidant activities. Objective: We investigated the neuroprotective effects of EAKS on ischemic damage in the gerbil hippocampal CA1 region after transient cerebral ischemia. Materials and methods: The ethanol extract of EAKS was obtained by organic solvent, collected in Kangwon province (South Korea) and orally administered using a feeding needle once a day for one week before transient cerebral ischemia in gerbils. Result: We adapted oral administration of 25 and 50 mg/kg EAKS because there are no data about the absorption and metabolism of EKAS. We found a significant neuroprotection in the 50 mg/kg EAKS-treated ischemia group, not in the 25 mg/kg EAKS-treated ischemia group, at 4 days ischemia-reperfusion (I-R). In the 50 mg/kg EAKS-treated ischemia group, about 68% of pyramidal neurons in the CA1 region were immunostained with neuronal nuclei (NeuN) 4 days after I-R, compared to the vehicle-treated ischemia group. 8-Hydroxy-2'-deoxyguanosine (a marker for DNA damage) and 4-hydroxy-2-nonenal (a marker for lipid peroxidation) immunoreactivity in the CA1 region of the EAKS-treated ischemia group were not markedly changed compared to the vehicle-treated ischemia group. In addition, Cu,Zn- and Mn-SOD immunoreactivity in the CA1 region of the EAKS-treated ischemia group were increased compared to the vehicle-treated ischemia group. Discussion: Repeated supplements of EAKS could protect neurons against ischemic damage, showing that DNA damage and lipid peroxidation are attenuated and SODs are increased in the ischemic CA1 region.Pharmaceutical Biology 10/2012; · 0.88 Impact Factor -
Article: Neuroprotective effects of Alpinia katsumadai against neuronal damage in the gerbil hippocampus induced by transient cerebral ischemia.
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ABSTRACT: Alpinia katsumadai, one of the family Zingiberaceae, contains chalcone, flavonoids, diarylheptanoids, monoterpenes, sesquiterpenoids, stilbenes, and labdanes. It has been reported that the extract of Alpinia katsumadai seed (EAKS) has antiinflammatory effects, and enhances antioxidant activities. We observed the neuroprotective effects of EAKS against ischemic damage in gerbils received oral administrations of EAKS (50 mg/kg) once a day for 7 days before transient cerebral ischemia. In the EAKS-treated ischemia group, neuronal nuclei (NeuN, a marker for neurons)-immunoreactive pyramidal neurons were abundant (68.3% of the sham group) in the hippocampal CA1 region (CA1) 4 days after ischemia/reperfusion (I/R) compared to those in the vehicle-treated ischemia group (13.18%). We also observed that EAKS treatment significantly decreased the activation of astrocytes and microglia in the CA1 compared with the vehicle-treated ischemia group 4 days postischemia. In addition, protein levels of GFAP and Iba-1 in the EAKS-treated ischemia group were much lower than those in the vehicle-treated ischemia group 4 days after I/P. Our findings indicate that the repeated supplements of EAKS could protect neurons from an ischemic damage, showing that glial activation is markedly decreased in the ischemic area.The International journal of neuroscience 09/2011; 121(9):490-6. · 0.86 Impact Factor -
Article: Ethyl acetate extracts of raw and steamed Codonopsis lanceolata protects against ischemic damage potentially by maintaining SOD1 and BDNF levels.
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ABSTRACT: We observed the neuroprotective effects of ECLs treatment on ischemic damage in the gerbil hippocampal CA1 region four days after an ischemic insult. Among the 10 ECLs, EERCL and EESCL showed significant neuroprotection: the percentage of neurons remaining after treatment with EERCL and EESCL was 72.7% and 68.4% of that seen in the sham-ischemia group, respectively. The administration of EERCL and EESCL significantly decreased the reactive gliosis of microglia compared with that seen in the vehicle-treated ischemia group. In addition, SOD1 and BDNF immunoreactivity in the EERCL- and EESCL-ischemia groups were markedly increased compared with that in the vehicle-treated ischemia group. These results suggest that the administration of EERCL and EESCL can reduce ischemic neuronal loss potentially by maintaining SOD1 and BDNF immunoreactivity in the ischemic hippocampal CA1 region.The International journal of neuroscience 06/2011; 121(9):503-9. · 0.86 Impact Factor -
Article: Neuroprotection of Alpinia katsumadai Seed Extract against Neuronal Damage in the Ischemic Gerbil Hippocampus is Linked to Altered Brain-Derived Neurotrophic Factor.
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ABSTRACT: The extract of Alpinia katsumadai, a member of the family Zingiberaceae, shows anti-inflammatory effects and antioxidant activity. We observed the neuroprotective effects of the extract from Alpinia katsumadai seed (EAKS) against ischemic damage in gerbils administered oral EAKS (25, and 50 mg/kg) once a day for 7 days before transient cerebral ischemia. In the 50 mg/kg EAKS-treated ischemia group, about 67% of neurons in the hippocampal CA1 region (CA1) survived after ischemia/reperfusion (I/R) based on cresyl violet staining. We observed that EAKS treatment significantly maintained brain-derived neurotrophic factor (BDNF) immunoreactivity in the ischemic CA1 region after I/R. In addition, protein levels of BDNF in the 50 mg/kg EAKS-treated ischemia group were much higher than those in the vehicle-treated ischemia group after I/R. These findings indicate that repeated supplementation of EAKS protects neurons from ischemic damage, such that BDNF is distinctively maintained in ischemic areas.Laboratory animal research. 03/2011; 27(1):67-71. -
Article: Chronic treatment of exendin-4 affects cell proliferation and neuroblast differentiation in the adult mouse hippocampal dentate gyrus.
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ABSTRACT: Exendin-4 isolated from Heloderma suspectum venom acts via glucagon-like peptide 1 (GLP-1) receptor and has clinically been used in the type 2 diabetes. In this study, we investigated the effects of exendin-4 on cell proliferation and neuroblast differentiation in the subgranular zone (SGZ) of the dentate gyrus in mice. Exendin-4 was treated intraperitoneally to male ICR mice twice a day for 21 days. The exendin-4-treated group showed a significantly higher number of Ki67- (1.51-fold), doublecortin (DCX)- (2.5-fold) and 5-bromo-2'-deoxyuridine (BrdU)+DCX- (2.46-fold) immunoreactive cells in the SGZ of the dentate gyrus compared to the control group. The results of this study showed that treatment with exendin-4 increased cell proliferation neuroblast differentiation in the SGZ of the dentate gyrus, suggesting that exendin-4 promotes structural plasticity in the dentate gyrus.Neuroscience Letters 12/2010; 486(1):38-42. · 2.11 Impact Factor -
Article: Transient cerebral ischemia induces active astrocytosis without distinct neuronal death in the gerbil main olfactory bulb: a long-term analysis.
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ABSTRACT: In the present study, we examined ischemia-induced neuronal and glial changes in the gerbil MOB at various time points during 60 days after 5 min of transient cerebral ischemia. The number of neuronal neuclei-immunoreactive neurons was not changed after ischemia/reperfusion (I/R). Myelin basic protein immunoreaction was well preserved after I/R. Five days after I/R, reactive form of GFAP-immunoreactive astrocytes began to increase in the external plexiform layer and granule cell layer: These reactive astrocytes peaked 10 days after I/R, thereafter, they decreased with time after I/R. Iba-1-immunoreactive microglia were ubiquitously distributed in all layers of the MOB. After I/R, significant changes in their morphology and immunoreactivity were not detected. The results of western blot analyses for GFAP, Iba-1 and MBP were similar to the immunohistochemical data. In addition, 8-hydroxy-2'-deoxyguanosine (a marker for DNA damage) immunoreactivity and SOD1, an antioxidant, protein levels were not changed in the ischemic MOB. These results indicate that neurons in the MOB are resistant to ischemic insult, showing that astrocytes are activated late in the ischemic MOB.Neurochemical Research 10/2010; 35(10):1588-98. · 2.24 Impact Factor -
Article: Comparison of newly generated doublecortin-immunoreactive neuronal progenitors in the main olfactory bulb among variously aged gerbils.
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ABSTRACT: In the present study, we investigated age-related differences in neuronal progenitors in the gerbil main olfactory bulb (MOB) using doublecortin (DCX), a marker for neuronal progenitors which differentiate into neurons in the brain. No difference in the number of neuronal nuclei (NeuN)-immunoreactive neurons was found in the MOB at variously aged gerbils. At postnatal month (PM) 1, DCX immunoreaction was detected in all layers of the MOB except for the olfactory nerve layer. At this time point, DCX-immunoreactive cells (neuronal progenitors) were very abundant; however, they did not have fully developed-processes. From PM 3, the number of DCX-immunoreactive neuronal progenitors was decreased with age. At PM 6, DCX-immunoreactive cells showed very well-developed processes. In western blot analysis, DCX protein level in the MOB was highest at PM 1. Thereafter, levels of DCX protein were decreased with age. In the subventricular zone of the lateral ventricle, the number of Ki-67-immunoractive cells (proliferating cells) was also significantly decreased with age. In addition, increases of α-synuclein-immunoreactive structures were observed in the MOB with age. These results suggest that decrease in DCX-immunoreactive neuronal progenitors and its protein levels in the MOB with age may be associated with reduction of cell proliferation in the SVZ and with an increase in α-synuclein in the MOB.Neurochemical Research 10/2010; 35(10):1599-608. · 2.24 Impact Factor -
Article: Maintenance of anti-inflammatory cytokines and reduction of glial activation in the ischemic hippocampal CA1 region preconditioned with lipopolysaccharide.
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ABSTRACT: Lipopolysaccharide (LPS) induces a strong immune response, and pretreatment with low dose of LPS suppresses the production of proinflammatory mediators. In the present study, we investigated the effect of LPS preconditioning on the delayed neuronal death in the gerbil hippocampal CA1 region after 5 min of transient cerebral ischemia. LPS preconditioning showed neuroprotective effects against ischemic damage in the hippocampal CA1 region after ischemic insult: about 92% of neurons in the CA1 region survived in the LPS-treated ischemia group. LPS preconditioning maintained anti-inflammatory cytokines, such as interleukin (IL)-4 and IL-13, in pyramidal neurons in the CA1 region after ischemia/reperfusion. In addition, IL-4 and IL-13 protein levels in the CA1 region of the LPS-treated ischemia group were similar to the vehicle-treated sham group. We found that reactive gliosis was markedly attenuated in the CA1 region of the LPS-treated ischemia group compared to the vehicle-treated ischemia group using immunohistochemistry of glial fibrillary acidic protein for astrocytes, and ionized calcium-binding adapter molecule 1 and isolectin B4 for microglia. These results indicate that LPS preconditioning may provide neuroprotection in the ischemic hippocampal CA1 region via maintenance of anti-inflammatory cytokines and suppression of glial activation.Journal of the neurological sciences 09/2010; 296(1-2):69-78. · 2.32 Impact Factor -
Article: Hypothyroid state does not protect but delays neuronal death in the hippocampal CA1 region following transient cerebral ischemia: focus on oxidative stress and gliosis.
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ABSTRACT: We investigated protective effects of hypothyroidism on delayed neuronal death, gliosis, lipid peroxidation and Cu,Zn-superoxide dismutase (SOD1) in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. The hypothyroidism was induced by 0.025% methimazole treatment. Free triiodothyronine and thyroxine levels were markedly decreased in the hypothyroid group. Four days after ischemia/reperfusion, only a few NeuN-immunoreactive (+) neurons were detected in the CA1 of euthyroid-ischemia (eu-ischemia) group; however, at this time point, the number of NeuN(+) neurons was significantly higher in the hypothyroid-ischemia (hypo-ischemia) group than in the eu-ischemia group. At 5 days postischemia, NeuN(+) neurons were significantly decreased in the hypo-ischemia group: The number of NeuN(+) neurons in this group was similar to that in the eu-ischemia group. Activations of GFAP(+) astrocytes and Iba-1(+) microglia in the CA1 were higher in the eu-ischemia group 3 and 4 days after ischemia/reperfusion. At 5 days postischemia, the activations of both the glial cells in the CA1 were similar between the two groups. 4-Hydroxy-2-nonenal (HNE), a marker for lipid peroxidation, immunoreactivity in the eu-ischemia group was higher than in the hypo-ischemia group; at 5 days postischemia, the immunoreactivity was similar between the two groups. In contrast, SOD1 level was lower in the CA1 of the eu-ischemia group. These results suggest that hypothyroid state does not protect against delayed neuronal death but only delays the neuronal death in the hippocampal CA1 region after transient cerebral ischemia by reducing lipid peroxidation and increasing SOD1.Journal of Neuroscience Research 09/2010; 88(12):2661-8. · 2.74 Impact Factor -
Article: Zizyphus attenuates ischemic damage in the gerbil hippocampus via its antioxidant effect.
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ABSTRACT: The fruit of Zizyphus jujuba has been used as a traditional Chinese medicinal herb and considered for thousands of years to affect various physiological functions in the body. We obtained a Z. jujuba extract (ZJE) and observed the neuroprotective effects of ZJE against ischemic damage in gerbils that had received repeated oral administrations of ZJE for 10 days. In the ZJE-treated ischemia group, neuronal nuclei (a marker for neurons)-immunoreactive neurons were abundant (58.4% vs. sham group) in the hippocampal CA1 region 4 days after ischemia/reperfusion compared to those in the vehicle-treated ischemia group (11.3%). In addition, ZJE treatment significantly decreased the reactive gliosis of astrocytes and microglia in the CA1 region compared to that in the vehicle-treated group 4 days after ischemia/reperfusion. Immunoreactivities of Cu,Zn-superoxide dismutase (SOD1) and brain-derived neurotrophic factor in the ZJE-treated ischemia group were higher those in the vehicle-treated ischemia group 4 days after ischemia/reperfusion. In addition, in the ZJE-treated ischemia group, levels of hydroxynonenal, an indicator of lipid peroxidation, were much lower than those in the vehicle-treated ischemia group after ischemia/reperfusion. These results suggest that the repeated supplements of ZJE can protect neurons from ischemic damage via up-regulation of SOD1 and reduction of lipid peroxidation in the ischemic hippocampal CA1 region.Journal of medicinal food 06/2010; 13(3):557-63. · 1.39 Impact Factor -
Article: Immunohistochemical changes in orexigenic and anorexigenic neuropeptides in the rat hypothalamus after capsaicin administration.
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ABSTRACT: Capsaicin has effects on the adiposity by increasing energy and lipid metabolism, and decreases appetite and fat intake. In the present study, we investigated changes in food intake and body weight after capsaicin treatment. We also observed changes in orexigenic and anorexigenic neuropeptides-agouti-related peptide (AgRP), alpha-melanocyte-stimulating hormone (alpha-MSH), adrenocorticotropic hormone (ACTH) and orexin-immunoreactivities in the rat hypothalamus after capsaicin administration. Only one day after capsaicin treatment, the mean food intake was significantly decreased. There was no significant difference in the mean body weight between vehicle- and capsaicin-treated groups. In addition, after capsaicin treatment, numbers of AgRP- and orexin-immunoreactive ((+)) cells were significantly decreased in the arcuate nucleus (ARC) and lateral hypothalamic area, respectively. In contrast, the number of alpha-MSH(+) and ACTH(+) cells in the ARC of the capsaicin-treated rats was higher than in the vehicle-treated rats. These results indicate that capsaicin reduces food intake, not body weight, transiently, and decreases AgRP and orexin immunoreactivities, whereas it increases alpha-MSH and ACTH immunoreactivities in rat hypothalamic nuclei.Journal of Veterinary Medical Science 10/2009; 71(10):1337-42. · 0.85 Impact Factor -
Article: Ischemia-related changes in naive and mutant forms of ubiquitin and neuroprotective effects of ubiquitin in the hippocampus following experimental transient ischemic damage.
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ABSTRACT: Ubiquitin binds to short-lived proteins and denatured proteins produced by various forms of injury. The loss of ubiquitin leads to an accumulation of abnormal proteins and may affect cellular structure and function. The aim of the present study is to observe the chronological changes in ubiquitin naive form and its mutant form (ubiquitin(+1)) in the hippocampal CA1 region (CA1) after transient cerebral ischemia in gerbils. Delayed neuronal death in the CA1 was confirmed 4 days after ischemic insult with NeuN immunohistochemistry. Ubiquitin immunoreactivity and protein level in the CA1 were lowest at 12 h after ischemia/reperfusion; thereafter, they were increased with time. Ubiquitin(+1) immunoreactivity and protein levels in the CA1 were slightly decreased at 3 h after ischemia/reperfusion, and they were significantly increased 1 day after ischemia/reperfusion. In addition, ubiquitin and ubiquitin(+1) immunoreaction was expressed in astrocytes after delayed neuronal death in the ischemic CA1. To elucidate the protective effect of ubiquitin on ischemic damage, the animals were treated with ubiquitin (1.5 mg/kg body weight) intravenously via the femoral vein. Ubiquitin treatment significantly reduced ischemia-induced locomotor hyperactivity, neuronal death and reactive gliosis such as astrocytes and microglia. In addition, 5 days after ubiquitin treatment in the ischemic group, ubiquitin immunoreactivity was similar to that in the ubiquitin-treated sham group, however, ubiquitin(+1) immunoreactivity was higher than that in the ubiquitin-treated sham group. These findings indicate that the depletion of ubiquitin and the accumulation of ubiquitin(+1) in CA1 pyramidal neurons after transient cerebral ischemia may inhibit ubiquitin proteolytic pathway and this leads to delayed neuronal death of CA1 pyramidal neurons directly or indirectly after transient cerebral ischemia.Experimental Neurology 09/2009; 220(1):120-32. · 4.70 Impact Factor -
Article: Neuroprotection of ebselen against ischemia/reperfusion injury involves GABA shunt enzymes.
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ABSTRACT: Seleno-organic compound, ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), is a substrate with radical-scavenging activity. In this study, we observed the neuroprotective effects of ebselen against ischemic damage and on GABA shunt enzymes such as glutamic acid decarboxylase 67 (GAD67), GABA transaminse (GABA-T) and succinic semialdehyde dehydrogenase (SSADH) in the hippocampal CA1 region after 5 min of transient forebrain ischemia in gerbils. For this, vehicle (physiological saline) or ebselen was administered 30 min before or after ischemia/reperfusion and sacrificed 4 days after ischemia/reperfusion. The administration of ebselen significantly reduced the neuronal death in the CA1 region induced by ischemia/reperfusion. In addition, treatment with ebselen markedly elevated GAD67, GABA-T and SSADH immunoreactivity and their protein levels compared to that in the vehicle-treated group, respectively. These results suggest that ebselen protects neurons from ischemic damage via control of the expressions of GABA shunt enzymes to enter the TCA cycle.Journal of the neurological sciences 08/2009; 285(1-2):88-94. · 2.32 Impact Factor -
Article: Indole-3-propionic acid attenuates neuronal damage and oxidative stress in the ischemic hippocampus.
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ABSTRACT: Tryptophan-derived indole compounds have been widely investigated as antioxidants and as free-radical scavengers. Indole-3-propionic acid (IPA), one of these compounds, is a deamination product of tryptophan. In the present study, we used Mongolian gerbils to investigate IPA's neuroprotective effects against ischemic damage and its antioxidative effects in the hippocampal CA1 region (CA1) after 5 min of transient forebrain ischemia. The repeated oral administration of IPA (10 mg/kg) for 15 days before ischemic surgery protected neurons from ischemic damage. In this group, the percentage of cresyl violet-positive neurons in the CA1 was 56.8% compared with that in the sham group. In the vehicle-treated group, glial fibrillary acidic protein (GFAP)-, S-100-, and vimentin-immunoreactive astrocytes and ionized calcium-binding adapter molecule 1 (Iba-1)- and isolectin B4 (IB4)-immunoreactive microglia were activated 4 days after ischemia/reperfusion, whereas in the IPA-treated ischemic group, GFAP, S-100, Iba-1, and IB4, but not vimentin, immunoreactivity was distinctly lower than that in the vehicle-treated ischemic groups. The administration of IPA significantly decreased the level of 4-hydroxy-2-nonenal, a marker of lipid peroxidation, in ischemic hippocampal homogenates compared with that in the vehicle-treated ischemic groups at various times after ischemia/reperfusion. In addition, immunostaining for 8-hydroxy-2'-deoxyguanosine showed DNA damage in pyramidal neurons in the ischemic CA1 was significantly lower in the IPA-treated ischemic groups than in the vehicle-treated ischemic groups. These results suggest that IPA protects neurons from ischemia-induced neuronal damage by reducing DNA damage and lipid peroxidation.Journal of Neuroscience Research 03/2009; 87(9):2126-37. · 2.74 Impact Factor -
Article: Indole‐3‐propionic acid attenuates neuronal damage and oxidative stress in the ischemic hippocampus
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ABSTRACT: Tryptophan-derived indole compounds have been widely investigated as antioxidants and as free-radical scavengers. Indole-3-propionic acid (IPA), one of these compounds, is a deamination product of tryptophan. In the present study, we used Mongolian gerbils to investigate IPA's neuroprotective effects against ischemic damage and its antioxidative effects in the hippocampal CA1 region (CA1) after 5 min of transient forebrain ischemia. The repeated oral administration of IPA (10 mg/kg) for 15 days before ischemic surgery protected neurons from ischemic damage. In this group, the percentage of cresyl violet–positive neurons in the CA1 was 56.8% compared with that in the sham group. In the vehicle-treated group, glial fibrillary acidic protein (GFAP)-, S-100-, and vimentin-immunoreactive astrocytes and ionized calcium-binding adapter molecule 1 (Iba-1)– and isolectin B4 (IB4)–immunoreactive microglia were activated 4 days after ischemia/reperfusion, whereas in the IPA-treated ischemic group, GFAP, S-100, Iba-1, and IB4, but not vimentin, immunoreactivity was distinctly lower than that in the vehicle-treated ischemic groups. The administration of IPA significantly decreased the level of 4-hydroxy-2-nonenal, a marker of lipid peroxidation, in ischemic hippocampal homogenates compared with that in the vehicle-treated ischemic groups at various times after ischemia/reperfusion. In addition, immunostaining for 8-hydroxy-2′-deoxyguanosine showed DNA damage in pyramidal neurons in the ischemic CA1 was significantly lower in the IPA-treated ischemic groups than in the vehicle-treated ischemic groups. These results suggest that IPA protects neurons from ischemia-induced neuronal damage by reducing DNA damage and lipid peroxidation. © 2009 Wiley-Liss, Inc.Journal of Neuroscience Research 02/2009; 87(9):2126 - 2137. · 2.74 Impact Factor -
Article: Expression and changes of hyperoxidized peroxiredoxins in non-pyramidal and polymorphic cells in the gerbil hippocampus during normal aging.
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ABSTRACT: Oxidative stress is one of predisposing factors to age-related neurodegeneration in the brain. In particular, thiol-containing groups are susceptible to oxidative stress, which induces the formation of the disulfide bond and/or hyperoxidized form of thiol-containing proteins. We observed the protein thiol levels in the hippocampal homogenates and also investigated changes in hyperoxidized form of peroxiredoxin (Prx-SO(3)) immunoreactivity and proteins levels in the gerbil hippocampal subregions during normal aging. Levels of total thiol, non-protein thiol, and protein thiol were decreased in the hippocampal homogenates with age. At post-natal month 1 (PM 1), pyramidal and non-pyramidal cells in the hippocampal CA1 region (CA1) showed Prx-SO(3) immunoreactivity. Prx-SO(3) immunoreactivity in the cells was decreased by PM 12, thereafter, Prx-SO(3) immunoreactivity in the cells increased again with age. In the CA2/3, Prx-SO(3) immunoreactivity in pyramidal cells was not significantly changed; however, the immunoreactivity in pyramidal cells was very low at PM 12. Prx-SO(3) immunoreactivity in the dentate gyrus (DG) was distinctly changed during aging. At PM 1, Prx-SO(3) immunoreactivity in granule and polymorphic cells was weak and strong, respectively. The immunoreactivity in the neurons was decreased with age, not shown in any neurons at PM 12. Thereafter, Prx-SO(3) immunoreactivity increased again with age. In addition, Prx-SO(3) protein level in the hippocampus was lowest at PM 12. These results suggest that thiol-containing proteins are changed during aging and Prx-SO(3) immunoreactivity was different according to cells in the hippocampal subregion during aging.Cellular and Molecular Neurobiology 01/2009; 29(3):413-21. · 1.97 Impact Factor -
Article: Germinated Buckwheat extract decreases blood pressure and nitrotyrosine immunoreactivity in aortic endothelial cells in spontaneously hypertensive rats.
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ABSTRACT: Thee present study analysed the quantification of rutin in raw buckwheat extract (RBE) and germinated buckwheat extract (GBE) by high performance liquid chromatography (HPLC), and examined changes in body weight, systolic blood pressure (SBP) and nitrotyrosine (a marker for peroxynitrite formation) immunoreactivity in aortic endothelial cells in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats after treatment with RBE and GBE for 5 weeks. In the HPLC study, RBE and GBE contained a mean content of rutin of 1.52 +/- 0.21 and 2.92 +/- 0.88 mg/g, respectively. In the 600 mg/kg GBE-treated group, SBP was lower than that in the 600 mg/kg RBE-treated group. The treatment with RBE and/or GBE significantly reduced oxidative damage in aortic endothelial cells by lowering nitrotyrosine immunoreactivity. These results suggest that GBE has an antihypertensive effect and may protect arterial endothelial cells from oxidative stress.Phytotherapy Research 01/2009; 23(7):993-8. · 2.09 Impact Factor -
Article: Induction of cell proliferation and neuroblasts in the subgranular zone of the dentate gyrus by aqueous extract from Platycodon grandiflorum in middle-aged mice.
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ABSTRACT: In the present study, we observed the neurogenic effects of an aqueous extract from the root of Platycodon grandiflorum (EPG) in middle-aged (12-month-old) mice. For this, 100mg/kg EPG was administered orally to mice for 30 days before sacrifice and 5-bromodeoxyguanosine (BrdU) was injected intraperitoneally every 8h for 24h on the day prior to sacrifice. The increase of neurogenesis was estimated by immunohistochemical staining for cellular proliferation markers (BrdU and Ki67) and a marker for neuroblasts (Doublecortin, DCX). These markers were detected in the subgranular zone of the dentate gyrus in vehicle- and EPG-treated groups. The number of BrdU-, Ki67- and DCX-positive cells in the EPG-treated group was significantly increased compared to that in the vehicle-treated group. In addition, DCX-positive cells in the EPG-treated group showed well-developed processes. These results suggest that the number of neuroblasts is increased by the repeated treatment of EPG in middle-aged mice.Neuroscience Letters 11/2008; 444(1):97-101. · 2.11 Impact Factor -
Article: Changes in glial fibrillary acidic protein immunoreactivity in the dentate gyrus and hippocampus proper of adult and aged dogs.
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ABSTRACT: Astrocytes perform neuron-supportive tasks, repair and scarring process in the central nervous system. In this study, we observed glial fibrillary acidic protein (GFAP), a marker for astrocytes, immunoreactivity in the dentate gyrus and hippocampus proper (CA1-3 region) of adult (2-3 years of age) and aged (10-12 years of age) dogs. In the adult group, GFAP immunoreactive astrocytes were distributed in all layers of the dentate gyrus and CA1-3 region, except in the stratum pyramidale of the CA1-3 region. In the aged group, GFAP immunoreactivity decreased markedly in the molecular layer of the dentate gyrus. However, GFAP immunoreactivity in the CA1-3 region increased in all layers, and the cytoplasm of GFAP immunoreactive astrocytes was hypertrophied. GFAP protein levels in the aged dentate gyrus decreased; however, GFAP levels in the CA1-3 region increased. These results suggest that the morphology of astrocytes and GFAP protein levels in the hippocampal dentate gyrus and CA1 region are changed, respectively, with age.Journal of Veterinary Medical Science 10/2008; 70(9):965-9. · 0.85 Impact Factor -
Article: Transient increases of glutamic acid decarboxylase 67 immunoreactivity and its protein levels in the somatosensory cortex after transient cerebral ischemia in gerbils.
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ABSTRACT: In this study, we investigated changes in glutamic acid decarboxylase 67 (GAD67) immunoreactivity and its protein levels in the gerbil somatosensory cortex after ischemia/reperfusion. GAD67 immunoreactivity was significantly increased in layers III and V of the somatosensory cortex 12 hr after ischemia/reperfusion. Thereafter, GAD67 immunoreactivity was decreased with time after ischemia/reperfusion. GAD67 immunoreactivity in the somatosensory cortex 4 days after ischemia/reperfusion was similar to that in the sham-operated group. In addition, GAD67 protein levels were also significantly increased 12 hr after transient forebrain ischemia. These results suggest that the transient increase of GAD67 immunoreactivity in layers III and V may be associated with responses to transient ischemia-induced neuronal damage.Journal of Veterinary Medical Science 10/2008; 70(9):1005-10. · 0.85 Impact Factor
Top co-authors
Top Journals
Institutions
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2011–2012
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Kangwon National University
Syunsen, Gangwon, South Korea -
Gangneung-Wonju National University
Wŏnju, Gangwon, South Korea
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2006–2010
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Hallym University
- College of Medicine
Seoul, Seoul, South Korea
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2007–2009
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Seoul National University
- College of Veterinary Medicine
Seoul, Seoul, South Korea
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