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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 | 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 |
| 4 | 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 |
| 5 | Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia显示文摘Transient ischemia in the whole brain leads to neuronal loss/death in vulnerable brain regions. The striatum, neocortex and hippocampus selectively loose specific neurons after transient ischemia. Just 5 minutes of transient ischemia can cause pyramidal neuronal death in the hippocampal cornu ammonis (CA) 1 field at 4 days after transient ischemia. In this study, we investigated the effects of 5-minute (mild), 15-minute (severe), and 20-minute (lethal) transient ischemia by bilateral common carotid artery occlusion (BCCAO) on behavioral change and neuronal death and gliosis (astrocytosis and microgliosis) in gerbil hippocampal subregions (CA1-3 region and dentate gyrus). We performed spontaneous motor activity test to evaluate gerbil locomotor activity, cresyl violet staining to detect cellular distribution, neuronal nuclei immunohistochemistry to detect neuronal distribution, and Fluoro-Jade B histofluorescence to evaluate neuronal death. We also conducted immunohistochemical staining for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 (Ibal) to evaluate astrocytosis and microgliosis, respectively. Animals subjected to 20-minute BCCAO died in at least 2 days. BCCAO for 15 minutes led to pyramidal cell death in hippocampal CA1-3 region 2 days later and granule cell death in hippocampal de匚tate gyrus 5 days later. Similar results were not found in animals subjected to 5-minute BCCAO. Gliosis was much more rapidly and severely progressed in animals subjected to 15-minute BCCAO than in those subjected to 5- minute BCCAO. Our results indicate that neuronal loss in the hippocampal formation following transient ischemia is significantly different according to regions and severity of transient ischemia. The experimental protocol was approved by Institutional Animal Care and Use Committee (AICUC) of Kangwon National University (approval No. KW-180124-1) on May 22, 2018. | Tae-Kyeong Lee Hyunjung Kim Minah Song Jae-Chul Lee Joon Ha Park Ji Hyeon Ahn Go Eun Yang Hyeyoung Kim Taek Geun Ohk Myoung Cheol Shin Jun Hwi Cho Moo-Ho Won | 2019 | Neural Regeneration Research2019，14，8： | 3 |
| 6 | Oenanthe Javanica Extract Protects Against Experimentally Induced Ischemic Neuronal Damage via its Antioxidant Effects显示文摘 | Joon Ha Park Jeong Hwi Cho In Hye Kim Ji Hyeon Ahn Jae-Chul Lee Bai Hui Chen Bich-Na Shin Hyun-Jin Tae Ki-Yeon Yoo SeongKweon Hong II Jun Kang Moo-Ho Won Jong-Dai Kim | 2015 | Chinese Medical Journal2015，，21： | 2 |
| 7 | Activation of immediate-early response gene c-Fos protein in the rat paralimbic cortices after myocardial infarction显示文摘c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, Neu N immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction. | Ji Yun Ahn Hyun-Jin Tae Jeong-Hwi Cho In Hye Kim Ji Hyeon Ahn Joon Ha Park Dong Won Kim Jun Hwi Cho Moo-Ho Won Seongkweon Hong Jae-Chul Lee Jeong Yeol Seo | 2015 | Neural Regeneration Research2015，10，8： | 2 |
| 8 | MicroRNA‐196A‐2 polymorphisms and hepatocellular carcinoma in patients with chronic hepatitis B显示文摘 | Hwi Young Kim Jung‐Hwan Yoon Hyo‐Suk Lee Jae Youn Cheong Sung Won Cho Hyoung Doo Shin Yoon Jun Kim | 2014 | J Med Virol2014，，3： | 1 |
| 9 | Ethanol extract of Oenanthe javanica increases cell proliferation and neuroblast differentiation in the adolescent rat dentate gyrus显示文摘Oenanthe javanica is an aquatic perennial herb that belongs to the Oenanthe genus in Apiaceae family, and it displays well-known medicinal properties such as protective effects against glutamate-induced neurotoxicity. However, few studies regarding effects of Oenanthe javanica on neurogenesis in the brain have been reported. In this study, we examined the effects of a normal diet and a diet containing ethanol extract of Oenanthe javanica on cell proliferation and neuroblast differentiation in the subgranular zone of the hippocampal dentate gyrus of adolescent rats using Ki-67(an endogenous marker for cell proliferation) and doublecortin(a marker for neuroblast). Our results showed that Oenanthe javanica extract significantly increased the number of Ki-67-immunoreactive cells and doublecortin-immunoreactive neuroblasts in the subgranular zone of the dentate gyrus in the adolescent rats. In addition, the immunoreactivity of brain-derived neurotrophic factor was significantly increased in the dentate gyrus of the Oenanthe javanica extract-treated group compared with the control group. However, we did not find that vascular endothelial growth factor expression was increased in the Oenanthe javanica extract-treated group compared with the control group. These results indicate that Oenanthe javanica extract improves cell proliferation and neuroblast differentiation by increasing brain-derived neurotrophic factor immunoreactivity in the rat dentate gyrus. | Bai Hui Chen Joon Ha Park Jeong Hwi Cho In Hye Kim Bich Na Shin Ji Hyeon Ahn Seok Joon Hwang Bing Chun Yan Hyun Jin Tae Jae Chul Lee Eun Joo Bae Yun Lyul Lee Jong Dai Kim Moo-Ho Won Il Jun Kang | 2015 | Neural Regeneration Research2015，10，2： | 1 |
| 10 | Decreased Insulin-Like Growth Factor-I and Its Receptor Expression in the Hippocampus and Somatosensory Cortex of the Aged Mouse显示文摘 | Choong Hyun Lee Ji Hyeon Ahn Joon Ha Park Bing Chun Yan In Hye Kim Dae Hwan Lee Jeong-Hwi Cho Bai Hui Chen Jae-Chul Lee Jun Hwi Cho Yun Lyul Lee Moo-Ho Won Il-Jun Kang | 2014 | Neurochemical Research2014，，4： | 1 |
| 11 | MicroRNA‐196A‐2 polymorphisms and hepatocellular carcinoma in patients with chronic hepatitis B显示文摘 | Hwi Young Kim Jung‐Hwan Yoon Hyo‐Suk Lee Jae Youn Cheong Sung Won Cho Hyoung Doo Shin Yoon Jun Kim | 2014 | J. Med. Virol2014，，3： | 1 |
| 12 | Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia显示文摘Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest(CA). In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet(CV) and Fluore-Jade B(F-J B) staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1(Iba-1), glial fibrillary acidic protein(GFAP), and tumor necrosis factor-alpha(TNF-α) immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA(about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA). Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated(enlarged cell bodies with short and thicken processes) in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region. | Hyun-Jin Tae Il Jun Kang Tae-Kyeong Lee Jeong Hwi Cho Jae-Chul Lee Myoung Cheol Shin Yoon Sung Kim Jun Hwi Cho Jong-Dai Kim Ji Hyeon Ahn Joon Ha Park In-Shik Kim Hyang-Ah Lee Yang Hee Kim Moo-Ho Won Young Joo Lee | 2017 | Neural Regeneration Research2017，12，12： | 1 |
| 13 | Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death显示文摘Long-term administration of scopolamine, a muscarinic receptor antagonist, can inhibit the survival of newly generated cells, but its effect on the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus remain poorly understood. In this study, we used immunohistochemistry and western blot methods to weekly detect the biological behaviors of nerve cells in the hippocampal dentate gyrus of adult mice that received intraperitoneal administration of scopolamine for 4 weeks. Expression of neuronal nuclear antigen(Neu N; a neuronal marker) and Fluoro-Jade B(a marker for the localization of neuronal degeneration) was also detected. After scopolamine treatment, mouse hippocampal neurons did not die, and Ki-67(a marker for proliferating cells)-immunoreactive cells were reduced in number and reac hed the lowest level at 4 weeks. Doublecortin(DCX; a marker for newly generated neurons)-immunoreactive cells were gradually shortened in length and reduced in number with time. After scopolamine treatment for 4 weeks, nearly all of the 5-bromo-2′-deoxyuridine(Brd U)-labeled newly generated cells were located in the subgranular zone of the dentate gyrus, but they did not migrate into the granule cell layer. Few mature Brd U/Neu N double-labeled cells were seen in the subgranular zone of the dentate gyrus. These findings suggest that long-term administration of scopolamine interferes with the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus, but it does not induce cell death. | Bing Chun Yan Joon Ha Park Bai Hui Chen Jeong-Hwi Cho In Hye Kim Ji Hyeon Ahn Jae-Chul Lee In Koo Hwang Jun Hwi Cho Yun Lyul Lee Il-Jun Kang Moo-Ho Won | 2014 | Neural Regeneration Research2014，9，19： | 0 |
| 14 | Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia显示文摘Monocarboxylate transporters(MCTs), which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning(IPC) on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups(sham-operated group, ischemia only group, IPC + sham-operated group and IPC + ischemia group). A serious loss of neuron was found in the stratum pyramidale of the hippocampal CA1 region(CA1), not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC + ischemia groups, neurons in the stratum pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the stratum pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the stratum pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC + sham-operated group, MCT4 immunoreactivity in the stratum pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC + ischemia group, MCT4 immunoreactivity was also increased in the stratum pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the stratum pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia. | Seongkweon Hong Ji Yun Ahn Geum-Sil Cho In Hye Kim Jeong Hwi Cho Ji Hyeon Ahn Joon Ha Park Moo-Ho Won Bai Hui Chen Bich-Na Shin Hyun-Jin Tae Seung Min Park Jun Hwi Cho Soo Young Choi Jae-Chul Lee | 2015 | Neural Regeneration Research2015，10，10： | 0 |
| 15 | Delayed hippocampal neuronal death in young gerbil following transient global cerebral ischemia is related to higher and longer-term expression of p63 in the ischemic hippocampus显示文摘The tumor suppressor p63 is one of p53 family members and plays a vital role as a regulator of neuronal apoptosis in the development of the nervous system. However, the role of p63 in mature neuronal death has not been addressed yet. In this study, we first compared ischemia-induced effects on p63 expression in the hippocampal regions(CA1–3) between the young and adult gerbils subjected to 5 minutes of transient global cerebral ischemia. Neuronal death in the hippocampal CA1 region of young gerbils was significantly slow compared with that in the adult gerbils after transient global cerebral ischemia. p63 immunoreactivity in the hippocampal CA1 pyramidal neurons in the sham-operated young group was significantly low compared with that in the sham-operated adult group. p63 immunoreactivity was apparently changed in ischemic hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. In the ischemia-operated adult groups, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons was significantly decreased at 4 days post-ischemia; however, p63 immunoreactivity in the ischemia-operated young group was significantly higher than that in the ischemia-operated adult group. At 7 days post-ischemia, p63 immunoreactivity was decreased in the hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. Change patterns of p63 level in the hippocampal CA1 region of adult and young gerbils after ischemic damage were similar to those observed in the immunohistochemical results. These findings indicate that higher and longer-term expression of p63 in the hippocampal CA1 region of the young gerbils after ischemia/reperfusion may be related to more delayed neuronal death compared to that in the adults. | Eun Joo Bae Bai Hui Chen Bing Chun Yan Bich Na Shin Jeong Hwi Cho In Hye Kim Ji Hyeon Ahn Jae Chul Lee Hyun-Jin Tae Seongkweon Hong Dong Won Kim Jun Hwi Cho Yun Lyul Lee Moo-Ho Won Joon Ha Park | 2015 | Neural Regeneration Research2015，10，6： | 0 |
| 16 | Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia显示文摘Ischemic preconditioning(IPC) is a condition of sublethal transient global ischemia and exhibits neuroprotective effects against subsequent lethal ischemic insult.We,in this study,examined the neuroprotective effects of IPC and its effects on immunoreactive changes of antioxidant enzymes including superoxide dismutase(SOD) 1 and SOD2,catalase(CAT) and glutathione peroxidase(GPX) in the gerbil hippocampal CA1 region after transient forebrain ischemia.Pyramidal neurons of the stratum pyramidale(SP) in the hippocampal CA1 region of animals died 5 days after lethal transient ischemia without IPC(8.6%(ratio of remanent neurons) of the sham-operated group);however,IPC prevented the pyramidal neurons from subsequent lethal ischemic injury(92.3%(ratio of remanent neurons) of the sham-operated group).SOD1,SOD2,CAT and GPX immunoreactivities in the sham-operated animals were easily detected in pyramidal neurons in the stratum pyramidale(SP) of the hippocampal CA1 region,while all of these immunoreactivities were rarely detected in the stratum pyramidale at 5 days after lethal transient ischemia without IPC.Meanwhile,their immunoreactivities in the sham-operated animals with IPC were similar to(SOD1,SOD2 and CAT) or higher(GPX) than those in the sham-operated animals without IPC.Furthermore,their immunoreactivities in the stratum pyramidale of the ischemia-operated animals with IPC were steadily maintained after lethal ischemia/reperfusion.Results of western blot analysis for SOD1,SOD2,CAT and GPX were similar to immunohistochemical data.In conclusion,IPC maintained or increased the expression of antioxidant enzymes in the stratum pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain ischemia and IPC exhibited neuroprotective effects in the hippocampal CA1 region against transient forebrain ischemia. | Seung Min Park Chan Woo Park Tae-Kyeong Lee Jeong Hwi Cho Joon Ha Park Jae-Chul Lee Bai Hui Chen Bich-Na Shin Ji Hyeon Ahn Hyun-Jin Tae Myoung Cheol Shin Taek Geun Ohk Jun Hwi Cho Moo-Ho Won Soo Young Choi In Hye Kim | 2016 | Neural Regeneration Research2016，11，7： | 0 |
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