• Proceedings of the PSK Conference
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• 2001.10a
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• pp.158.2-158
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• 2001

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.141.2-142
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• 2002

• Biomolecules & Therapeutics
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• v.23 no.3
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• pp.261-267
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• 2015

Pioglitazone (PGZ), a synthetic peroxisome proliferator-activated receptor ${\gamma}$ agonist, is known to regulate inflammatory process and to have neuroprotective effects against neurological disorders. In the present study, we examined the effects of 30 mg/kg PGZ on excitotoxic neuronal damage and glial activation in the mouse hippocampus following intracerebroventricular injection of kainic acid (KA). PGZ treatment significantly reduced seizure-like behavior. PGZ had the neuroprotective effect against KA-induced neuronal damage and attenuated the activations of astrocytes and microglia in the hippocampal CA3 region. In addition, MPO and $NF{\kappa}B$ immunoreactivities in the glial cells were also decreased in the PGZ-treated group. These results indicate that PGZ had anticonvulsant and neuroprotective effects against KA-induced excitotocix injury, and that neuroprotective effect of PGZ might be due to the attenuation of KA-induced activation in astrocytes and microglia as well as KA-induced increases in MPO and $NF{\kappa}B$.

• BMB Reports
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• v.49 no.11
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• pp.635-640
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• 2016

Recent evidence indicates that the ephrin receptors and ephrin ligands (Eph/ephrin) expression modulate axonal reorganization and synaptic plasticity in stroke recovery. To investigate the effect of task-specific training (TST) on Eph/ephrin expression in the corticospinal tract (CST) after stroke, we compared Eph/ephrin expression in the peri-infarct cortex, pyramid, and spinal cord of a photothrombotic stroke model of rat brains treated with or without TST. The TST treatment showed significantly better recovery in the behavioral tests compared with no treatment. The significant upregulation of ephrin-A1 and ephrin-A5 observed in activated astrocytes of the CST at 2 weeks' post-stroke was decreased by TST. At 5 weeks, post-stroke, the elevated ephrin-A5 levels were decreased in the ipsilateral pyramid and spinal cord by TST. Glial fibrillary acidic protein was upregulated concomitantly with the altered ephrin expression after stroke, and the expression of these proteins was attenuated by TST. These data suggest that TST alters the expression of ephrin ligands in the CST after stroke.

• Journal of Genetic Medicine
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• v.10 no.2
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• pp.88-93
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• 2013

Alexander disease (ALXD) is a rare demyelinating disease of the white matter of the brain that is caused by a mutation in the glial fibrillary acidic protein (GFAP) gene. The overexpression of GFAP in astrocytes induces a failure in the developmental growth of the myelin sheath. The neurodegenerative destruction of the myelin sheath of the white matter is accompanied by an accumulation of abnormal deposits of Rosenthal fibers in astrocytes, which is the hallmark of ALXD. The disease can be divided into four groups based on the onset age of the patients: neonatal, infantile, juvenile, or adult. Early-onset disease is more severe, progresses rapidly, and results in a shorter life span than late-onset cases. Magnetic resonance imaging and genetic tests are mostly used for diagnostic purposes. Pathological tests of brain tissue for Rosenthal fibers are definitive diagnostic methods. Therapeutic strategies are being investigated. Ceftriaxone, which is an enhancer of glial glutamate transporter (GLT-1) expression, is currently in clinical trials for the treatment of patients with ALXD. To date, there are no clinically available treatments. The cause, pathology, pathophysiology, inheritance, clinical features, diagnosis, and treatment of ALXD will be reviewed comprehensively.

• Journal of Oriental Neuropsychiatry
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• v.20 no.2
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• pp.31-46
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• 2009

Objectives : This experiment was designed to investigate the effect of Gojineumja(Guzhenyinzi, GJEJ) on damaged neural tissue in cultured glial cells and in the mouse brain tissue. Methods : The effects of the GJEJ on activation of astrocytes and caspase 3-positive cell counts in cultured glial cells administered with ${\beta}$-amyloid peptide were investigated. The effects of the GJEJ on levels of glial fibrillary acidic protein(GFAP)-positive reactive astrocyets and caspase 3-positive cells in the hippocampal subfields in the rats administered with scopolamine were investigated. Results : 1. GJEJ reduced levels of activated astrocytes and caspase 3-positive cell counts in cultured glial cells administered with ${\beta}$-amyloid peptide. 2. GJEJ reduced levels of GFAP-positive reactive astrocyets and caspase 3-positive cells in the hippocampal subfields in the rats administered with scopolamine. Conclusions : The present data. suggest that GJEJ may have a protective function of neuronal and non-neuronal cells in damaged neural tissue caused by AD-like stimulations. Further studies on identification of effective molecular components of GJEJ and their interactions with damaged neural cells would be important for understanding molecular mechanism and may be further applicable for the development of therapeutic strategies.

• Journal of Ginseng Research
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• v.28 no.2
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• pp.120-126
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• 2004

Glial cells such as astrocytes and microglial cells are the main source of proinflammatory cytokines and nitric oxide(NO) in the central nervous system, which exert neuroimmune and inflammatory functions and other various neurobiologic effects. Though Panax ginseng C.A. Meyer has been known to strengthen the body's defence mechanisms and also to maintain the homeostasis in the central nervous system, the effects of Panax ginseng on the production of immune and inflammatory mediators have not been studied well in the brain. Therefore, this study was designed to study the effects of ginseng saponins on the production of proinflammatory cytokines and NO in the primary cultures of mixed glial cells. White ginseng saponin, 200-500 $\mu$g/ml, showed significant cytotoxicity after 72 hrs and increased TNF-$\alpha$, IL-$\beta$, and NO production. Lower doses of 50-100 $\mu\textrm{g}$/ml showed little cytotoxicity until 72 hrs and also increased the production of TNF-$\alpha$, IL-1$\beta$, and NO. Triple immune staining showed that white ginseng saponin, 200$\mu\textrm{g}$/ml for 72 ks, induced stellation of astrocytes and iNOS expression exclusively in microglial cells. Taken together, the white ginseng saponin increased the production of proinflammatory cytokines such as TNF-$\alpha$ and IL-1$\beta$, and induced iNOS expression and NO production in mixed glial cell cultures, which may be ascribed to the enhancement of central immune responses and the regulation of inflammatory reactions by Panax ginseng.

• Journal of fish pathology
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• v.7 no.1
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• pp.63-70
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• 1994

Nitric oxide(NO) has recently been shown to play an important role on central nervous system(CNS) function in mammals. It is synthesized from L-arginine by the enzyme NO synthase. In this study, we examined this enzyme's existence in CNS of rainbow trout(Oncorhynchus mykiss) and described the forms of microglia. astrocytes. and oligodendrocytes. Two forms of microglia are distributed in CNS. one resembling their mammalian counterpart(large microglia : LM). and the other comprising small microglia(SM) with very little cytoplasm. CNS contained astrocytes of a distinct type which form reticular network, but lack connections to capillaries. The oligodendrocyte was generally a much denser cell than the astrocyte. We have detected NOS($1.04{\pm}0.12\;pg/min/mg$) from rainbow trout CNS. It could be inhibited reversibly or irreversibly by $N^{G}MMA$ and EGTA. These result suggest that the formation of NO from L-arginine in CNS is calcium-dependent and a pathway of early evolutionary orgin.

• Biomolecules & Therapeutics
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• v.26 no.5
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• pp.439-445
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• 2018

T-type calcium channels are low voltage-activated calcium channels that evoke small and transient calcium currents. Recently, T-type calcium channels have been implicated in neurodevelopmental disorders such as autism spectrum disorder and neural tube defects. However, their function during embryonic development is largely unknown. Here, we investigated the function and expression of T-type calcium channels in embryonic neural progenitor cells (NPCs). First, we compared the expression of T-type calcium channel subtypes (CaV3.1, 3.2, and 3.3) in NPCs and differentiated neural cells (neurons and astrocytes). We detected all subtypes in neurons but not in astrocytes. In NPCs, CaV3.1 was the dominant subtype, whereas CaV3.2 was weakly expressed, and CaV3.3 was not detected. Next, we determined CaV3.1 expression levels in the cortex during early brain development. Expression levels of CaV3.1 in the embryonic period were transiently decreased during the perinatal period and increased at postnatal day 11. We then pharmacologically blocked T-type calcium channels to determine the effects in neuronal cells. The blockade of T-type calcium channels reduced cell viability, and induced apoptotic cell death in NPCs but not in differentiated astrocytes. Furthermore, blocking T-type calcium channels rapidly reduced AKT-phosphorylation (Ser473) and $GSK3{\beta}$-phosphorylation (Ser9). Our results suggest that T-type calcium channels play essential roles in maintaining NPC viability, and T-type calcium channel blockers are toxic to embryonic neural cells, and may potentially be responsible for neurodevelopmental disorders.

• Korean Journal of Veterinary Research
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• v.33 no.2
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• pp.295-300
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• 1993

Central nervous system of two dogs with natural canine distemper was investigated histopathologically and immunocytochemically with antisera to MBP, MAG and GFAP. Histopathologically, there were neuronal degeneration and diffuse gliosis in the cerebrum, vacuolar degeneration, hypertrophy of astrocytes and demyelination in cerebellar white matter adjacent to the 4th ventricle and optic tracts showing non-inflammatory demyelinating encephalomyelitis (Summers and Appel, 1987). Immunohistochemically, there was a concurrent disappearance of MBP and MAG in the well developed demyelinating lesion in the cerebellar white matter. At the margin of demyelination, Loss of both MBP and MAG varied on the stage of demyelinating process. GFAP-positive astrocytes were hypertrophied and contained canine distemper virus intranuclear inclusions. GFAP-positive fibers were increased at the early stage of demyelination, and then were not immunoreaeted at the well developed demyelination. Hypertrophic astrocytes with intranuclear inclusions were commonly identified in the interfascular layer without myelin vacuolation and demyelination. This is the first study of primary demyelination and astroglial reactions in natural CDE investigated using immunocytochemistry of two myelin proteins and GFAP. Concurrent loss of MBP and MAG suggest that the myelin sheath is the target in the demyelinating process in CDE.