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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>
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>
Increased immunoreactivity of c???Fos in the spinal cord of the aged mouse and dog.
Ahn, Ji Hyeon,Shin, Myoung Chul,Park, Joon Ha,Kim, In Hye,Lee, Jae-Chul,Yan, Bing Chun,Hwang, In Koo,Moon, Seung Myung,Ahn, Ji Yun,Ohk, Taek Geun,Lee, Tae Hun,Cho, Jun Hwi,Shin, Hyung-Cheul,Won, Moo-H SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.11 No.2
<P>Expression of c-Fos in the spinal cord following nociceptive stimulation is considered to be a neurotoxic biomarker. In the present study, the immunoreactivity of c-Fos in the spinal cord was compared between young adult (2-3 years in dogs and 6 months in mice) and aged (10-12 years in dogs and 24 months in mice) Beagle dogs and C57BL/6J mice. In addition, changes to neuronal distribution and damage to the spinal cord were also investigated. There were no significant differences in neuronal loss or degeneration of the spinal neurons observed in either the aged dogs or mice. Weak c-Fos immunoreactivity was observed in the spinal neurons of the young adult animals; however, c-Fos immunoreactivity was markedly increased in the nuclei of spinal neurons in the aged dogs and mice, as compared with that of the young adults. In conclusion, c-Fos immunoreactivity was significantly increased without any accompanying neuronal loss in the aged spinal cord of mice and dogs, as compared with the spinal cords of the young adult animals.</P>
Ahn, Ji Hyeon,Shin, Myoung Cheol,Park, Joon Ha,Kim, In Hye,Cho, Jeong-Hwi,Lee, Tae-Kyeong,Lee, Jae-Chul,Chen, Bai Hui,Shin, Bich Na,Tae, Hyun-Jin,Park, Jinseu,Choi, Soo Young,Lee, Yun Lyul,Kim, Dae Wo SPANDIDOS PUBLICATIONS 2017 MOLECULAR MEDICINE REPORTS Vol.15 No.6
<P>Therapeutic exercise is an integral component of the rehabilitation of patients who have suffered a stroke. The objective of the present study was to use immunohistochemistry to investigate the effects of post-ischemic exercise on neuronal damage or death and gliosis in the aged gerbil hippocampus following transient cerebral ischemia. Aged gerbils (male; age, 22–24 months) underwent ischemia and were subjected to treadmill exercise for 1 or 4 weeks. Neuronal death was detected in the stratum pyramidale of the hippocampal CA1 region and in the polymorphic layer of the dentate gyrus using cresyl violet and Fluoro-Jade B histofluorescence staining. No significant difference in neuronal death was identified following 1 or 4 weeks of post-ischemic treadmill exercise. However, post-ischemic treadmill exercise affected gliosis (the activation of astrocytes and microglia). Glial fibrillary acidic protein-immunoreactive astrocytes and ionized calcium binding adaptor molecule 1-immunoreactive microglia were activated in the CA1 and polymorphic layer of the dentate gyrus of the group without treadmill exercise. Conversely, 4 weeks of treadmill exercise significantly alleviated ischemia-induced astrocyte and microglial activation; however, 1 week of treadmill exercise did not alleviate gliosis. These findings suggest that long-term post-ischemic treadmill exercise following transient cerebral ischemia does not influence neuronal protection; however, it may effectively alleviate transient cerebral ischemia-induced astrocyte and microglial activation in the aged hippocampus.</P>
Ahn, Ji Hyeon,Shin, Myoung Cheol,Kim, Dae Won,Kim, Hyunjung,Song, Minah,Lee, Tae-Kyeong,Lee, Jae-Chul,Kim, Hyeyoung,Cho, Jun Hwi,Kim, Young-Myeong,Kim, Jong-Dai,Choi, Soo Young,Won, Moo-Ho,Park, Joon MDPI 2019 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.20 No.3
<P>Fucoidan, a natural sulfated polysaccharide, displays various biological activities including antioxidant properties. We examined the neuroprotective effect of fucoidan against transient global cerebral ischemia (tGCI) in high-fat diet (HFD)-induced obese gerbils and its related mechanisms. Gerbils received HFD for 12 weeks and fucoidan (50 mg/kg) daily for the last 5 days during HFD exposure, and they were subjected to 5-min tGCI. Pyramidal cell death was observed only in the CA 1 area (CA1) of the hippocampus in non-obese gerbils 5 days after tGCI. However, in obese gerbils, pyramidal cell death in the CA1 and CA2/3 occurred at 2 days and 5 days, respectively, after tGCI. In the obese gerbils, oxidative stress indicators (dihydroethidium, 8-hydroxyguanine and 4-hydroxy-2-nonenal) were significantly enhanced and antioxidant enzymes (SOD1 and SOD2) were significantly reduced in pre- and post-ischemic phases compared to the non-obese gerbils. Fucoidan treatment attenuated acceleration and exacerbation of tGCI-induced neuronal death in the CA1–3, showing that oxidative stress was significantly reduced, and antioxidant enzymes were significantly increased in pre- and post-ischemic phases. These findings indicate that pretreated fucoidan can relieve the acceleration and exacerbation of ischemic brain injury in an obese state via the attenuation of obesity-induced severe oxidative damage.</P>