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| 1 | Pretreated Glehnia littoralis Extract Prevents Neuronal Death Following Transient Global Cerebral Ischemia through Increases of Superoxide Dismutase 1 and Brain-derived Neurotrophic Factor Expressions in the Gerbil Hippocampal Cornu Ammonis 1 Area显示文摘 | Joon Ha Park Tae-Kveono Lee Bing-Chun Yan Bich-Na Shin Ji Hyeon Ahn In Hye Kim Jeong Hwi Cho Jae-Chul Lee In Koo Hwang Jong Dai Kim Seongkweon Hong Young Joo Lee Moo-Ho Woll Il Jun Kang | 2017 | Chinese Medical Journal2017，，15： | 10 |
| 2 | Pretreated quercetin protects gerbil hippocampal CA1 pyramidal neurons from transient cerebral ischemic injury by increasing the expression of antioxidant enzymes显示文摘Quercetin(QE; 3,5,7,3′,4′-pentahydroxyflavone), a well-known flavonoid, has been shown to prevent against neurodegenerative disorders and ischemic insults. However, few studies are reported regarding the neuroprotective mechanisms of QE after ischemic insults. Therefore, in this study, we investigated the effects of QE on ischemic injury and the expression of antioxidant enzymes in the hippocampal CA1 region of gerbils subjected to 5 minutes of transient cerebral ischemia. QE was pre-treated once daily for 15 days before ischemia. Pretreatment with QE protected hippocampal CA1 pyramidal neurons from ischemic injury, which was confirmed by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, pretreatment with QE significantly increased the expression levels of endogenous antioxidant enzymes Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase in the hippocampal CA1 pyramidal neurons of animals with ischemic injury. These findings demonstrate that pretreated QE displayed strong neuroprotective effects against transient cerebral ischemia by increasing the expression of antioxidant enzymes. | Bai Hui Chen Joon Ha Park Ji Hyeon Ahn Jeong Hwi Cho In Hye Kim Jae Chul Lee Moo-Ho Won Choong-Hyun Lee In Koo Hwang Jong-Dai Kim Il Jun Kang Jun Hwi Cho Bich Na Shin Yang Hee Kim Yun Lyul Lee Seung Min Park | 2017 | Neural Regeneration Research2017，12，2： | 9 |
| 3 | Neuroprotection via maintenance or increase of antioxidants and neurotrophic factors in ischemic gerbil hippocampus treated with tanshinone I显示文摘 | Joon Ha Park Ok kyu Park Yah Bingchun Ji Hyeon Ahn In Hye Kim Jae-Chul Lee Seung-Hae Kwon Ki-Yeon Yoo Choong Hyun Lee In Koo Hwang Jung Hoon Choi Moo-Ho Won Jong-Dai Kim | 2014 | Chinese Medical Journal2014，，19： | 8 |
| 4 | Glehnia fittoralis Extract Promotes Neurogenesis in the Hippocampal Dentate Gyrus of the Adult Mouse through Increasing Expressions of Brain-Derived Neurotrophic Factor and Tropomyosin-Related Kinase B显示文摘 | Joon Ha Park Bich Na Shin Ji Hyeon Ahn Jeong Hwi Cho Tae-Kyeong Lee Jae-Chul Lee Yong Hwan Jeon II Jun Kang Ki-Yeon Yoo In Koo Hwang Choong Hyun Lee Yoo Hun Noh Sung-Su Kim Moo-Ho Won Jong Dai Kim | 2018 | Chinese Medical Journal2018，，6： | 6 |
| 5 | Pretreated Oenan the Javanica extract increases anti-inflammatory cytokines, attenuates gliosis, and protects hippocampal neurons following transient global cerebral ischemia in gerbils显示文摘Recently,we have reported that Oenanthe javanica extract(OJE)displays strong neuroprotective effect against ischemic damage after transient global cerebral ischemia.However,neuroprotective mechanisms of OJE have not been fully identified.Thus,this study investigated the neuroprotection of OJE in the hippocampal CA1 area and its anti-inflammatory activity in gerbils subjected to 5 minutes of transient global cerebral ischemia.We treated the animals by intragastrical injection of OJE(100 and 200 mg/kg)once daily for 1 week prior to transient global cerebral ischemia.Neuroprotection of OJE was observed by immunohistochemistry for neuronal nuclear antigen and histofluorescence staining for Fluoro-Jade B.Immunohistochemistry of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 was done for astrocytosis and microgliosis,respectively.To investigate the neuroprotective mechanisms of OJE,we performed immunohistochemistry of tumor necrosis factor-alpha and interleukin-2 for pro-inflammatory function and interleukin-4 and interleukin-13 for anti-inflammatory function.When we treated the animals by intragastrical administration of 200 mg/kg of OJE,hippocampal CA1 pyramidal neurons were protected from transient global cerebral ischemia and cerebral ischemia-induced gliosis was inhibited in the ischemic hippocampal CA1 area.We also found that interleukin-4 and-13 immunoreactivities were significantly increased in pyramidal neurons of the ischemic CA1 area after OJE pretreatment,and the increased immunoreactivities were sustained in the CA1 pyramidal neurons after transient global cerebral ischemia.However,OJE pretreatment did not increase interleukin-2 and tumor necrosis factor-alpha immunoreactivities in the CA1 pyramidal neurons.Our findings suggest that pretreatment with OJE can protect neurons and attenuate gliosis from transient global cerebral ischemia via increasing expressions of interleukin-4 and-13.The experimental plan of this study was reviewed and approved by the Institutional Animal Care and Use Committee(IACUC)in Kangwon National University(approval No.KW-160802-1)on August 10,2016. | Joon Ha Park In Hye Kim Ji Hyeon Ahn YooHun Noh Sung-Su Kim Tae-Kyeong Lee Jae-Chul Lee Bich-Na Shin Tae Heung Sim Hyun Sam Lee Jeong Hwi Cho In Koo Hwang Il Jun Kang Jong Dai Kim Moo-Ho Won | 2019 | Neural Regeneration Research2019，14，9： | 6 |
| 6 | Glucose metabolism and neurogenesis in the gerbil hippocampus after transient forebrain ischemia显示文摘Recent evidence exists that glucose transporter 3(GLUT3) plays an important role in the energy metabolism in the brain.Most previous studies have been conducted using focal or hypoxic ischemia models and have focused on changes in GLUT3 expression based on protein and m RNA levels rather than tissue levels.In the present study,we observed change in GLUT3 immunoreactivity in the adult gerbil hippocampus at various time points after 5 minutes of transient forebrain ischemia.In the sham-operated group,GLUT3 immunoreactivity in the hippocampal CA1 region was weak,in the pyramidal cells of the CA1 region increased in a time-dependent fashion 24 hours after ischemia,and in the hippocampal CA1 region decreased significantly between 2 and 5 days after ischemia,with high level of GLUT3 immunoreactivity observed in the CA1 region 10 days after ischemia.In a double immunofluorescence study using GLUT3 and glial-fibrillary acidic protein(GFAP),we observed strong GLUT3 immunoreactivity in the astrocytes.GLUT3 immunoreactivity increased after ischemia and peaked 7 days in the dentate gyrus after ischemia/reperfusion.In a double immunofluorescence study using GLUT3 and doublecortin(DCX),we observed low level of GLUT3 immunoreactivity in the differentiated neuroblasts of the subgranular zone of the dentate gyrus after ischemia.GLUT3 immunoreactivity in the sham-operated group was mainly detected in the subgranular zone of the dentate gyrus.These results suggest that the increase in GLUT3 immunoreactivity may be a compensatory mechanism to modulate glucose level in the hippocampal CA1 region and to promote adult neurogenesis in the dentate gyrus. | Dae Young Yoo Kwon Young Lee Joon Ha Park Hyo Young Jung Jong Whi Kim Yeo Sung Yoon Moo-Ho Won Jung Hoon Choi In Koo Hwang | 2016 | Neural Regeneration Research2016，11，8： | 4 |
| 7 | Beta-nerve growth factor gene therapy alleviates pyridoxine-induced neuropathic damage by increasing doublecortin and tyrosine kinase A in the dorsal root ganglion显示文摘Beta-nerve growth factor(β-NGF)is known to be a major leading cause of neuronal plasticity.To identify the possible action mechanisms ofβ-NGF gene therapy for sciatic nerve recovery,experimental dogs were randomly divided into control,pyridoxine,and pyridoxine+β-NGF groups.We observed chronological changes of morphology in the dorsal root ganglia in response to pyridoxine toxicity based on cresyl violet staining.The number of large neurons positive for cresyl violet was dramatically decreased after pyridoxine intoxication for 7 days in the dorsal root ganglia and the neuron number was gradually increased after pyridoxine withdrawal.In addition,we also investigated the effects ofβ-NGF gene therapy on neuronal plasticity in pyridoxine-induced neuropathic dogs.To accomplish this,tyrosine kinase receptor A(TrkA),βIII-tubulin and doublecortin(DCX)immunohistochemical staining was performed at 3 days after the last pyridoxine treatment.TrkA-immunoreactive neurons were dramatically decreased in the pyridoxine group compared to the control group,but strong TrkA immunoreactivity was observed in the small-sized dorsal root ganglia in this group.TrkA immunoreactivity in the dorsal root ganglia was similar betweenβ-NGF and control groups.The numbers ofβⅢ-tubulin-and DCX-immunoreactive cells decreased significantly in the pyridoxine group compared to the control group.However,the reduction ofβⅢ-tubulin-and DCX-immunoreactive cells in the dorsal root ganglia in theβ-NGF group was significantly ameliorated than that in the pyridoxine group.These results indicate thatβ-NGF gene therapy is a powerful treatment of pyridoxine-induced neuropathic damage by increasing the TrkA and DCX levels in the dorsal root ganglia.The experimental protocol was approved by the Institutional Animal Care and Use Committee(IACUC)of Seoul National University,South Korea(approval No.SNU-060623-1,SNU-091009-1)on June 23,2006 and October 9,2009,respectively. | Hyun-Kee Cho Woosuk Kim Kwon-Young Lee Jin-Ok Ahn Jung Hoon Choi In Koo Hwang Jin-Young Chung | 2020 | Neural Regeneration Research2020，15，1： | 2 |
| 8 | Time- and cell-type specific changes in iron, ferritin, and transferrin in the gerbil hippocampal CA1 region after transient forebrain ischemia显示文摘In the present study, we used immunohistochemistry and western blot analysis to examine changes in the levels and cellular localization of iron, heavy chain ferritin(ferritin-H), and transferrin in the gerbil hippocampal CA1 region from 30 minutes to 7 days following transient forebrain ischemia. Relative to sham controls, iron reactivity increased significantly in the stratum pyramidale and stratum oriens at 12 hours following ischemic insult, transiently decreased at 1–2 days and then increased once again within the CA1 region at 4–7 days after ischemia. One day after ischemia, ferritin-H immunoreactivity increased significantly in the stratum pyramidale and decreased at 2 days. At 4–7 days after ischemia, ferritin-H immunoreactivity in the glial components in the CA1 region was significantly increased. Transferrin immunoreactivity was increased significantly in the stratum pyramidale at 12 hours, peaked at 1 day, and then decreased significantly at 2 days after ischemia. Seven days after ischemia, Transferrin immunoreactivity in the glial cells of the stratum oriens and radiatum was significantly increased. Western blot analyses supported these results, demonstrating that compared to sham controls, ferritin H and transferrin protein levels in hippocampal homogenates significantly increased at 1 day after ischemia, peaked at 4 days and then decreased. These results suggest that iron overload-induced oxidative stress is most prominent at 12 hours after ischemia in the stratum pyramidale, suggesting that this time window may be the optimal period for therapeutic intervention to protect neurons from ischemia-induced death. | Dae Young Yoo Ki-Yeon Yoo Joon Ha Park Hyun Jung Kwon Hyo Young Jung Jong Whi Kim Goang-Min Choi Seung Myung Moon Dae Won Kim Yeo Sung Yoon Moo-Ho Won In Koo Hwang | 2016 | Neural Regeneration Research2016，11，6： | 2 |
| 9 | Hypothyroidism affects astrocyte and microglial morphology in type 2 diabetes显示文摘In the present study,we investigated the effects of hypothyroidism on the morphology of astrocytes and microglia in the hippocampus of Zucker diabetic fatty rats and Zucker lean control rats.To induce hypothyroidism,Zucker lean control and Zucker diabetic fatty rats at 7 weeks of age orally received the vehicle or methimazole,an anti-thyroid drug,treatment for 5 weeks and were sacrificed at 12 weeks of age in all groups for blood chemistry and immunohistochemical staining.In the methimazole-treated Zucker lean control and Zucker diabetic fatty rats,the serum circulating triiodothyronine(T3)and thyroxine(T4)levels were significantly decreased compared to levels observed in the vehicle-treated Zucker lean control or Zucker diabetic fatty rats.This reduction was more prominent in the methimazole-treated Zucker diabetic fatty group.Glial fibrillary acidic protein immunoreactive astrocytes and ionized calcium-binding adapter molecule 1(Iba-1)-immunoreactive microglia in the Zucker lean control and Zucker diabetic fatty group were diffusely detected in the hippocampal CA1 region and dentate gyrus.There were no significant differences in the glial fibrillary acidic protein and Iba-1 immunoreactivity in the CA1 region and dentate gyrus between Zucker lean control and Zucker diabetic fatty groups.However,in the methimazole-treated Zucker lean control and Zucker diabetic fatty groups,the processes of glial fibrillary acidic protein immunoreactive astrocytes and Iba-1 immunoreactive microglia,were significantly decreased in both the CA1region and dentate gyrus compared to that in the vehicle-treated Zucker lean control and Zucker diabetic fatty groups.These results suggest that diabetes has no effect on the morphology of astrocytes and microglia and that hypothyroidism during the onset of diabetes prominently reduces the processes of astrocytes and microglia. | Sung Min Nam Yo Na Kim Dae Young Yoo Sun Shin Yi Jung Hoon Choi In Koo Hwang Je Kyung Seong Yeo Sung Yoon | 2013 | Neural Regeneration Research2013，8，26： | 2 |
| 10 | Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils显示文摘Calbindin D-28K(CB), a Ca2+-binding protein, maintains Ca2+ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We investigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei(Neu N) and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia(39.5 ± 0.2°C) was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neuronal damage/death in the pyramidal layer of CA1–3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreactivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immunoreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults. | Jae-Chul Lee Jeong-Hwi Cho Tae-Kyeong Lee In Hye Kim Moo-Ho Won Geum-Sil Cho Bich-Na Shin In Koo Hwang Joon Ha Park Ji Hyeon Ahn Il Jun Kang Young Joo Lee Yang Hee Kim | 2017 | Neural Regeneration Research2017，12，9： | 2 |
| 11 | Hippophae rhamnoides L.leaves extract enhances cell proliferation and neuroblast differentiation through upregulation of intrinsic factors in the dentate gyrus of the aged gerbil显示文摘 | Ji Hyeon Ahn Bai Hui Chen Joon Ha Park In Hye Kim Jeong-Hwi Cho Jae-Chul Lee Bing Chun Yan Jung Hoon Choi In Koo Hwang Ju-Hee Park Sang-No Han Yun Lyul Lee Myong Jo Kim Moo-Ho Won | 2014 | Chinese Medical Journal2014，，23： | 1 |
| 12 | Effects of treadmill exercise on cyclooxygenase-2 in the hippocampus in type 2 diabetic rats: Correlation with the neuroblasts 显示文摘 | Hwang In Koo Yi Sun Shin Yoo Ki-Yeon | 2010 | Brain Research2010，1341，： | 1 |
| 13 | Time-course of changes in phosphorylated CREB in neuroblasts and BDNF in the mouse dentate gyrus at early postnatal stages 显示文摘 | In Koo Hwang Ki-Yeon Yoo Dae Young Yoo | 2011 | Cell Mol Neurobiol2011，31，5： | 1 |
| 14 | Effects of fluoxetine on ischemic cells and expressions in BDNF and some antioxidants in the gerbil hippocampal CA1 region induced by transient ischemia显示文摘 | Do Hoon Kim Hua Li Ki-Yeon Yoo Bong-Hee Lee In Koo Hwang Moo Ho Won | 2007 | Experimental Neurology2007，，2： | 1 |
| 15 | Vanillin, 4-hydroxybenzyl aldehyde and 4-hydroxybenzyl alcohol prevent hippocampal CA1 cell death following global is- chemia显示文摘 | Hyeon Ju Kim In Koo Hwang Moo Ho Won | 2007 | Brain Res2007，1181，： | 1 |
| 16 | Vanillin, 4-hydroxybenzyl aldehyde and 4-hydroxybenzyl alcohol prevent hippocampal CA1 cell death following global ischemia显示文摘 | Hyeon Ju Kim In Koo Hwang Moo Ho Won | 2007 | Brain Research2007，，： | 1 |
| 17 | Leptin’s neuroprotective action in experimental transient ischemic damage of the gerbil hippocampus is linked to altered leptin receptor immunoreactivity显示文摘 | Bing Chun Yan Jung Hoon Choi Ki-Yeon Yoo Choong Hyun Lee In Koo Hwang Sang Guan You Il-Jun Kang Jong-Dai Kim Dae-joong Kim Young-Myeong Kim Moo-Ho Won | 2011 | Journal of the Neurological Sciences2011，，1： | 1 |
| 18 | Increase in Trx2/Prx3 redox system immunoreactivity in the spinal cord and hippocampus of aged dogs显示文摘 | Ji Hyeon Ahn Jung Hoon Choi Ju Min Song Choong Hyun Lee Ki-Yeon Yoo In Koo Hwang Jin Sang Kim Hyung-Cheul Shin Moo-Ho Won | 2011 | Experimental Gerontology2011，，11： | 1 |
| 19 | Chronological changes of N-methyl-D-aspartate receptors and excitatory amino acid carrier 1 immunoreactivities in CA1 area and subiculum after transient forebrain ischemia显示文摘 | Tae-Cheon Kang In Koo Hwang Seung-Kook Park Sung-Jin An Dae-Kun Yoon Seung Myung Moon Yoon-Bok Lee Heon-Soo Sohn Sa Sun Cho Moo Ho Won | 2001 | Journal of Neurocytology2001，，12： | 1 |
| 20 | (2004) In Vivo Protein Transduetion: Biologically Active Intact Pep-l-Superoxide Dismutase Fusion Protein Efficiently Protects Againtst Ischemic Insult显示文摘 | Won Sik Eum Dae Won Kim In Koo Hwang | 2004 | Free Radic Biol2004，137，10： | 1 |
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