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AHN, JI HYEON,NOH, YOOHUN,SHIN, BICH NA,KIM, SUNG-SU,PARK, JOON HA,LEE, TAE-KYEONG,SONG, MINAH,KIM, HYUNJUNG,LEE, JAE-CHUL,YONG, JUN-HWAN,KANG, IL JUN,LEE, YUN LYUL,WON, MOO-HO,KIM, JONG DAI SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.18 No.6
<P> Intermittent fasting has been shown to have neuroprotective effects against transient focal cerebral ischemic insults. However, the effects of intermittent fasting on transient global ischemic insult has not been studied much yet. The present study examined effects of intermittent fasting on endogenous antioxidant enzyme expression levels in the hippocampus and investigated whether the fasting protects neurons 5 days after 5 min of transient global cerebral ischemia. Gerbils were randomly subjected to either ad libitum or alternate?day intermittent fasting for two months and assigned to sham surgery or transient ischemia. Changes of antioxidant enzymes were examined using immunohistochemistry for cytoplasmic superoxide dismutase 1 (SOD1), mitochondrial (SOD2), catalase (CAT), and glutathione peroxidase (GPX). The effects of intermittent fasting on ischemia?induced antioxidant changes, neuronal damage/degeneration and glial activation were examined. The weight of fasting gerbils was not different from that of control gerbils. In controls, SOD1 and GPX immunoreactivities were strong in pyramidal neurons of filed cornu ammonis 1 (CA1). Transient ischemia in controls significantly decreased expressions of SOD1 and GPX in CA1 pyramidal neurons. Intermittent fasting resulted in increased expressions of SOD2 and CAT, not of SOD1 and GPX, in CA1 pyramidal neurons. Nevertheless, CA1 pyramidal neurons were not protected in gerbils subjected to fasting after transient ischemia, and inhibition of glial-cell activation was not observed in the gerbils. In summary, intermittent fasting for two months increased SOD2 and CAT immunoreactivities in hippocampal CA1 pyramidal neurons. However, fasting did not protect the CA1 pyramidal neurons from transient cerebral ischemia. The results of the present study indicate that intermittent fasting may increase certain antioxidants, but not protect neurons from transient global ischemic insult. </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>
Ahn, Ji Hyeon,Park, Joon Ha,Yan, Bing Chun,Lee, Jae-Chul,Choi, Jung Hoon,Lee, Choong Hyun,Yoo, Ki-Yeon,Hwang, In Koo,Kim, Jin Sang,Shin, Hyung-Cheul,Won, Moo-Ho Kluwer Academic/Plenum Publishers 2013 Cellular and molecular neurobiology Vol.33 No.1
<P>Alpha-synuclein (α-syn), as a neuroprotein, is expressed in neural tissue, and it is related to a synaptic transmission and neuronal plasticity. In this study, we compared the distribution and immunoreactivity of α-syn and related gliosis in hippocampus between young adult (2-3?years) and aged (10-12?years) beagle dogs. In both groups, α-syn immunoreactivity was detected in neuropil of all the hippocampal sub-regions, but not in neuronal somata. In the aged hippocampus, α-syn immunoreactivity was apparently increased in mossy fibers compared to that in the adult dog. In addition, α-syn protein level was markedly increased in the aged hippocampus. On the other hand, GFAP and Iba-1 immunoreactivity in astrocytes and microglia, respectively, were increased in all the hippocampal sub-regions of the aged group compared to that in the adult group: especially, their immunoreactivity was apparently increased around mossy fibers. In addition, in this study, we could not find any expression of α-syn in astrocytes and microglia. These results indicate that α-syn immunoreactivity apparently increases in the aged hippocampus and that GFAP and Iba-1 immunoreactivity are also apparently increased at the regions with increased α-syn immunoreactivity. This increase in α-syn expression might be a feature of normal aging.</P>
Ahn, Ji Hyeon,Chen, Bai Hui,Park, Joon Ha,Shin, Bich Na,Lee, Tae-Kyeong,Cho, Jeong Hwi,Lee, Jae Chul,Park, Jeong-Ran,Yang, Se-Ran,Ryoo, Sungwoo,Shin, Myoung Cheol,Cho, Jun Hwi,Kang, Il Jun,Lee, Choong Wiley (John WileySons) 2018 JOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MED Vol.12 No.7
<P>There is lack of researches on effects of intravenously injected mesenchymal stem cells (MSCs) against transient cerebral ischemia (TCI). We investigated the disruption of the neurovascular unit (NVU), which comprises the blood-brain barrier and examined entry of human dermis-derived MSCs (hDMSCs) into the damaged hippocampal CA1 area in a gerbil model of TCI and their subsequent effects on neuroprotection and cognitive function. Impairments of neurons and blood-brain barrier were examined by immunohistochemistry, electron microscopy, and Evans blue and immunoglobulin G leakage. Neuronal death was observed in pyramidal neurons 5-day postischemia. NVU were structurally damaged; in particular, astrocyte end-feet were severely damaged from 2-day post-TCI and immunoglobulin G leaked out of the CA1 area 2days after 5min of TCI; however, Evans blue extravasation was not observed. On the basis of the results of NVU damages, ischemic gerbils received PKH2-transfected hDMSCs 3 times at early times (3hr, 2, and 5days) after TCI, and fluorescence imaging was used to detect hDMSCs in the tissue. PKH2-transfected hDMSCs were not found in the CA1 from immediate time to 8days after injection, although they were detected in the liver. Furthermore, hDMSCs transplantation did not protect CA1 pyramidal neurons and did not improve cognitive impairment. Intravenously transplanted hDMSCs did not migrate to the damaged CA1 area induced by TCI. These findings suggest no neuroprotection and cognitive improvement by intravenous hDMSCs transplantation after 5min of TCI.</P>
Age-dependent decrease of Nurr1 protein expression in the gerbil hippocampus
Ahn, Ji Hyeon,Lee, Joon Seok,Cho, Jun Hwi,Park, Joon Ha,Lee, Tae-Kyeong,Song, Minah,Kim, Hyunjung,Kang, Seok Hoon,Won, Moo-Ho,Lee, Choong Hyun D.A. Spandidos 2018 Biomedical reports Vol.8 No.6
<P>Nuclear receptor related-1 protein (Nurr1) serves important roles in hippocampal-dependent cognitive process. In the present study, the protein expression of Nurr1 was compared in the hippocampi of young [postnatal month 3 (PM 3)], adult (PM 12) and aged (PM 24) gerbils using western blot analysis and immunohistochemistry. Results indicated that the protein level of Nurr1 was significantly and gradually decreased in the gerbil hippocampus with increasing age. In addition, strong Nurr1 immunoreactivity was primarily observed in pyramidal neurons and granule cells of the hippocampus in the young group, which was determined to be reduced in the adult group and to a greater extent in the aged group. Collectively the data demonstrated that Nurr1 immunoreactivity was gradually and markedly decreased during normal aging. These results indicate that gradual decrease of Nurr1 expression in the hippocampus may be associated with the normal aging process and a decline in hippocampus-dependent cognitive function.</P>