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Ahn, Ji Hyeon,Hong, Seongkweon,Park, Joon Ha,Kim, In Hye,Cho, Jeong Hwi,Lee, Tae-Kyeong,Lee, Jae-Chul,Chen, Bai Hui,Shin, Bich-Na,Bae, Eun Joo,Jeon, Yong Hwan,Kim, Young-Myeong,Won, Moo-Ho,Choi, Soo Y SPANDIDOS PUBLICATIONS 2017 MOLECULAR MEDICINE REPORTS Vol. No.
<P>Calbindin-D28k (CB), calretinin (CR) and parvalbumin (PV), which regulate cytosolic free Ca<SUP>2+</SUP> concentrations in neurons, are chemically expressed in γ-aminobutyric acid (GABA)ergic neurons that regulate the degree of glutamatergic excitation and output of projection neurons. The present study investigated age-associated differences in CB, CR and PV immunoreactivities in the somatosensory cortex in three species (mice, rats and gerbils) of young (1 month), adult (6 months) and aged (24 months) rodents, using immunohistochemistry and western blotting. Abundant CB-immunoreactive neurons were distributed in layers II and III, and age-associated alterations in their number were different according to the species. CR-immunoreactive neurons were not abundant in all layers; however, the number of CR-immunoreactive neurons was the highest in all adult species. Many PV-immunoreactive neurons were identified in all layers, particularly in layers II and III, and they increased in all layers with age in all species. The present study demonstrated that the distribution pattern of CB-, CR- and PV-containing neurons in the somatosensory cortex were apparently altered in number with normal aging, and that CB and CR exhibited a tendency to decrease in aged rodents, whereas PV tended to increase with age. These results indicate that CB, CR and PV are markedly altered in the somatosensory cortex, and this change may be associated with normal aging. These findings may aid the elucidation of the mechanisms of aging and geriatric disease.</P>
Park, Joon Ha,Cho, Jeong Hwi,Kim, In Hye,Ahn, Ji Hyeon,Lee, Jae-Chul,Chen, Bai Hui,Shin, Bich-Na,Tae, Hyun-Jin,Yoo, Ki-Yeon,Hong, SeongKweon,Kang, Il Jun,Won, Moo-Ho,Kim, Jong-Dai Medknow PublicationsMedia Pvt Ltd 2015 Chinese medical journal : CMJ Vol.128 No.21
<P><B>Background:</B></P><P>Water dropwort (<I>Oenanthe javanica</I>) as a popular traditional medicine in Asia shows various biological properties including antioxidant activity. In this study, we firstly examined the neuroprotective effect of <I>Oenanthe javanica</I> extract (OJE) in the hippocampal cornus ammonis 1 region (CA1 region) of the gerbil subjected to transient cerebral ischemia.</P><P><B>Methods:</B></P><P>Gerbils were established by the occlusion of common carotid arteries for 5 min. The neuroprotective effect of OJE was estimated by cresyl violet staining. In addition, 4 antioxidants (copper, zinc superoxide dismutase [SOD], manganese SOD, catalase, and glutathione peroxidase) immunoreactivities were investigated by immunohistochemistry.</P><P><B>Results:</B></P><P>Pyramidal neurons in the CA1 region showed neuronal death at 5 days postischemia; at this point in time, all antioxidants immunoreactivities disappeared in CA1 pyramidal neurons and showed in many nonpyramidal cells. Treatment with 200 mg/kg, not 100 mg/kg, OJE protected CA1 pyramidal neurons from ischemic damage. In addition, 200 mg/kg OJE treatment increased or maintained antioxidants immunoreactivities. Especially, among the antioxidants, glutathione peroxidase immunoreactivity was effectively increased in the CA1 pyramidal neurons of the OJE-treated sham-operated and ischemia-operated groups.</P><P><B>Conclusion:</B></P><P>Our present results indicate that treatment with OJE can protect neurons from transient ischemic damage and that the neuroprotective effect may be closely associated with increased or maintained intracellular antioxidant enzymes by OJE.</P>
Ahn, Ji Yun,Tae, Hyun-Jin,Cho, Jeong-Hwi,Kim, In Hye,Ahn, Ji Hyeon,Park, Joon Ha,Kim, Dong Won,Cho, Jun Hwi,Won, Moo-Ho,Hong, Seongkweon,Lee, Jae-Chul,Seo, Jeong Yeol Medknow PublicationsMedia Pvt Ltd 2015 Neural regeneration research Vol.10 No.8
<P>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, NeuN 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.</P>
Bae, Eun Joo,Chen, Bai Hui,Yan, Bing Chun,Shin, Bich Na,Cho, Jeong Hwi,Kim, In Hye,Ahn, Ji Hyeon,Lee, Jae Chul,Tae, Hyun-Jin,Hong, Seongkweon,Kim, Dong Won,Cho, Jun Hwi,Lee, Yun Lyul,Won, Moo-Ho,Park, Medknow PublicationsMedia Pvt Ltd 2015 Neural regeneration research Vol.10 No.6
<P>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.</P>
Ahn, Ji Hyeon,Chen, Bai Hui,Yan, Bing Chun,Park, Joon Ha,Kang, Il Jun,Lee, Tae-Kyeong,Cho, Jeong Hwi,Shin, Bich-Na,Lee, Jae-Chul,Jeon, Yong Hwan,Hong, Seongkweon,Lee, Young Joo,Choi, Soo Young,Won, Mo SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.17 No.1
<P>GABAergic projections terminate on numerous hippocampal interneurons containing calcium binding proteins (CBPs), including calbindin D-28k (CB), calretinin (CR) and parvalbumin (PV). Memory deficits and expression levels of CB, CR, and PV were examined in the hippocampal subregions following systemic scopolamine (Scop; 1 mg/kg) treatment for 4 weeks in mice. Scop treatment induced significant memory deficits from 1 week after Scop treatment. CB, CR and PV immunoreactivities distributions were in hippocampal subregions [CA1 and CA3 regions, and the dentate gyrus (DG)]. CB immunoreactivity (CB<SUP>+</SUP>) was gradually decreased in all subregions until 2 weeks after Scop treatment, and CB<SUP>+</SUP> was decreased to the lowest level in all subregions at 3 and 4 weeks. CR<SUP>+</SUP> in the CA1 region was gradually decreased until 2 weeks and hardly observed at 3 and 4 weeks; in the CA3 region, CR<SUP>+</SUP> was not altered in all subregions at any time. In the DG, CR+ was gradually decreased until 2 weeks and lowest at 3 and 4 weeks. PV<SUP>+</SUP> in the CA1 region was not altered at 1 week, and gradually decreased from 2 weeks. In the CA3 region, PV<SUP>+</SUP> did not change in any subregions at any time. In the DG, PV<SUP>+</SUP> was not altered at 1 week, decreased at 2 weeks, and lowest at 3 and 4 weeks. In brief, Scop significantly decreased CBPs expressions in the hippocampus ≥3 weeks after the treatment although memory deficits had developed at 1 week. Therefore, it is suggested that Scop (1 mg/kg) must be systemically treated for ≥3 weeks to investigate changes in expression levels of CBPs in the hippocampus.</P>
Kim, In Hye,Jeon, Yong Hwan,Lee, Tae-Kyeong,Cho, Jeong Hwi,Lee, Jae-Chul,Park, Joon Ha,Ahn, Ji Hyeon,Shin, Bich-Na,Kim, Yang Hee,Hong, Seongkweon,Yan, Bing Chun,Won, Moo-Ho,Lee, Yun Lyul Medknow PublicationsMedia Pvt Ltd 2017 Neural regeneration research Vol.12 No.6
<P>Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning (2-minute transient cerebral ischemia) on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult (5-minute transient cerebral ischemia). A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.</P>
Park, Joon Ha,Lee, Tae-Kyeong,Yan, Bing-Chun,Shin, Bich-Na,Ahn, Ji Hyeon,Kim, In Hye,Cho, Jeong Hwi,Lee, Jae-Chul,Hwang, In Koo,Kim, Jong Dai,Hong, Seongkweon,Lee, Young Joo,Won, Moo-Ho,Kang, Il Jun Medknow PublicationsMedia Pvt Ltd 2017 Chinese medical journal : CMJ Vol.130 No.15
<P><B>Background:</B></P><P><I>Glehnia littoralis</I>, as a traditional herbal medicine to heal various health ailments in East Asia, displays various therapeutic properties including antioxidant effects. However, neuroprotective effects of <I>G. littoralis</I> against cerebral ischemic insults have not yet been addressed. Therefore, in this study, we first examined its neuroprotective effects in the hippocampus using a gerbil model of transient global cerebral ischemia (TGCI).</P><P><B>Methods:</B></P><P>Gerbils were subjected to TGCI for 5 min. <I>G. littoralis</I> extract (GLE; 100 and 200 mg/kg) was administrated orally once daily for 7 days before ischemic surgery. Neuroprotection was examined by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. Gliosis was observed by immunohistochemistry for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1. For neuroprotective mechanisms, immunohistochemistry for superoxide dismutase (SOD) 1 and brain-derived neurotrophic factor (BDNF) was done.</P><P><B>Results:</B></P><P>Pretreatment with 200 mg/kg of GLE protected pyramidal neurons in the cornu ammonis 1 (CA1) area from ischemic insult area (<I>F</I> = 29.770, <I>P</I> < 0.05) and significantly inhibited activations of astrocytes (<I>F</I> = 22.959, <I>P</I> < 0.05) and microglia (<I>F</I> = 44.135, <I>P</I> < 0.05) in the ischemic CA1 area. In addition, pretreatment with GLE significantly increased expressions of SOD1 (<I>F</I> = 28.561, <I>P</I> < 0.05) and BDNF (<I>F</I> = 55.298, <I>P</I> < 0.05) in CA1 pyramidal neurons of the sham- and ischemia-operated groups.</P><P><B>Conclusions:</B></P><P>Our findings indicate that pretreatment with GLE can protect neurons from ischemic insults, and we suggest that its neuroprotective mechanism may be closely associated with increases of SOD1 and BDNF expressions as well as attenuation of glial activation.</P>
Yoo, Ki-Yeon,Kim, In Hye,Cho, Jeong-Hwi,Ahn, Ji Hyeon,Park, Joon Ha,Lee, Jae-Chul,Tae, Hyun-Jin,Kim, Dae Won,Kim, Jong-Dai,Hong, Seongkweon,Won, Moo-Ho,Kang, Il Jun Medknow PublicationsMedia Pvt Ltd 2016 Neural regeneration research Vol.11 No.2
<P>In this study, we tried to verify the neuroprotective effect of <I>Chrysanthemum indicum</I> Linne (CIL) extract, which has been used as a botanical drug in East Asia, against ischemic damage and to explore the underlying mechanism involving the anti-inflammatory approach. A gerbil was given CIL extract for 7 consecutive days followed by bilateral carotid artery occlusion to make a cerebral ischemia/reperfusion model. Then, we found that CIL extracts protected pyramidal neurons in the hippocampal CA1 region (CA1) from ischemic damage using neuronal nucleus immunohistochemistry and Fluoro-Jade B histofluorescence. Accordingly, interleukin-13 immunoreactivities in the CA1 pyramidal neurons of CIL-pretreated animals were maintained or increased after cerebral ischemia/reperfusion. These findings indicate that the pre-treatment of CIL can attenuate neuronal damage/death in the brain after cerebral ischemia/reperfusion <I>via</I> an anti-inflammatory approach.</P>