• YAKHAK HOEJI
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• v.46 no.6
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• pp.398-404
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• 2002

A phytochemical study on the root of Cibotium barometz J. Smith led to the isolation of onitin (I), daucosterol (II) and a new compound (III). Compound III was characterized as 2-Ο-(9Z,12Z-octadecadienoyl)-3-Ο-[$\alpha$-D-galactopyranosyl-(1"-6")-Ο-$\beta$-D-galactopyranosyl] glycerol, named shinbarometin by $^1$H-, $^{13}$ C-NMR and LC/MS data. Compound III exerted an induced neuronal regeneration on nogo-A induced neuroblastoma cells.

• BMB Reports
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• v.48 no.11
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• pp.599-608
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• 2015

Regeneration, a process of reconstitution of the entire tissue, occurs throughout life in the olfactory epithelium (OE). Regeneration of OE consists of several stages: proliferation of progenitors, cell fate determination between neuronal and non-neuronal lineages, their differentiation and maturation. How the differentiated cell types that comprise the OE are regenerated, is one of the central questions in olfactory developmental neurobiology. The past decade has witnessed considerable progress regarding the regulation of transcription factors (TFs) involved in the remarkable regenerative potential of OE. Here, we review current state of knowledge of the transcriptional regulatory networks that are powerful modulators of the acquisition and maintenance of developmental stages during regeneration in the OE. Advance in our understanding of regeneration will not only shed light on the basic principles of adult plasticity of cell identity, but may also lead to new approaches for using stem cells and reprogramming after injury or degenerative neurological diseases.

• Journal of the Korea Convergence Society
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• v.7 no.2
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• pp.61-67
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• 2016

The olfactory system is an important model for the study of neuronal degeneration and regeneration, including neuronal diseases. When the olfactory sensory neurons are damaged by nerve injury or are exposed to environmental factors, they degenerate and are replaced by regenerating neurons. To monitor neuronal degeneration in living animal, we established an olfactory-specific GFP transgenic zebrafish. The effects of Triton X-100 or sodium acetate on the olfactory system were examined. A significant decrease in the number of GFP-positive olfactory sensory neurons was observed after chemical lesion. We found a recovery of GFP-positive neurons by 2 days posttreatment. From these results, we expect that further studies of olfactory degeneration and regeneration using this transgenic zebrafish will provide important advances for the study of neuronal degeneration and regeneration.

• Journal of Microbiology and Biotechnology
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• v.19 no.11
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• pp.1490-1495
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• 2009

The development of nanotechnology has penetrated the fields of biology and medicine, resulting in remarkable applications for tissue regeneration. In order to apply this technology to tissue engineering, we have developed nano-scaled 3D scaffolds consisting of growth factor-loaded heparin/poly(l-lysine) nanoparticles (NPs) attached to the surface of polymeric micro spheres via polyionic complex methods. Growth factor-loaded NPs were simply produced as polyelectrolyte complexes with diameters of 100-200 nm. They were then coated onto positively charged poly(lactic-co-glycolic acid) (PLGA) pretreated with polyethyleneimine to enable cell adhesion, proliferation, and stimulation of neurite outgrowth. Propidium iodide staining and $\beta$-tubulin analysis revealed that neuronal PC12 cells proliferated extensively, expressed significant amounts of b-tubulin, and showed well-structured neurite outgrowth on polymeric microspheres by stimulation with growth factors. These results suggest that cellular adhesion and biological functionality on prepared PLGA microspheres enabled terminal differentiation of neuronal cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.6
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• pp.1640-1646
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• 2005

An oriental medicinal drugs Jahageo (JHG, Hominis placenta) were examined to determine its effects on the responsiveness of central nervous system neurons after injury. We found that JHG was involved in neurite outgrowth of DRG sensory axons. JHG treatment also increased expression of axonal growth-associated protein GAP-43 in DRG sensory neurons after sciatic nerve injury and in the injured spinal cord. JHG treatment during the spinal cord injury increased induction levels of cell division cycle 2 (Cdc2) protein in DRG as well as in the spinal cord. Histochemical investigation showed that induced Cdc2 in the injured spinal cord was found in non-neuronal cells. These results suggest that JHG regulates activities of non-neuronal cells such as oligodendrocyte and astrocyte in responses to spinal cord injury and protects neuronal responsiveness after axonal damage.

• Proceedings of the Korean Society of Machine Tool Engineers Conference
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• 2005.05a
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• pp.3-8
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• 2005

We introduced mechanical stimuli and micropatterned substrate with micro fibers to investigate the effects of those on neurite outgrowth along with nerve growth factor (NGF) in vitro. Microfiber substrates were fabricated using an electrospinning process. And PC-12 cells cultured on substrates were simulated with nerver growth factor and laminar flow shear stress in a fluid flow system The results suggest that microfiber substrates and fluid-induced shear stress are promising for simulating neuronal regeneration in a desired direction.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.3
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• pp.285-296
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• 1997

Injury to brain transforms resting astrocytes to their reactive form, the hallmark of which is an increase in glial fibrillary acidic protein (GFAP), the major intermediate filament protein of their cell type. The overall glial response after brain injury is referred to as reactive gliosis. Glial-neuronal interaction is important for neuronal migration, neurite outgrowth and axonal guidance during ontogenic development. Although much attention has been given to glial regulation of neuronal development and regeneration, evidences also suggest a neuronal influence on glial cell differentiation, maturation and function. The aim of the present study was to analyze the effects of glial-hippocampal neuronal co-culture on GFAP expression in the co-cultured astrocytes. The following antibodies were used for double immunostaining chemistry; mouse monoclonal antibodies for confirm neuronal cells, rabbit anti GFAP antibodies for confirm astrocytes. Primary cultured astrocytes showed the typical flat polygonal morphology in culture and expressed strong GFAP and vimentin. Co-cultured hippocampal neurons on astrocytes had phase bright cell body and well branched neurites. About half of co-cultured astrocytes expressed negative or weak GFAP and vimentin. After 2 hour glutamate (0.5 mM) exposure of glial-neuronal co-culture, neuronal cells lost their neurites and most of astrocytes expressed strong CFAE and vimentin. In Western blot analysis, total GFAP and vimentin contents in co-cultured astrocytes were lower than those of primary cultured astrocytes. After glutamate exposure of glial-neuronal co-culture, GFAP and vimentin contents in astrocytes were increased to the level of primary cultured astrocytes. These results suggest that neuronal cell decrease GFAP expression in co-cultured astrocytes and hippocampal neuronal-glial co-culture can be used as a reactive gliosis model in vitro for studying GFAP expression of astrocytes.

• Animal cells and systems
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• v.12 no.4
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• pp.203-209
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• 2008

Berberine, an isoquinoline alkaloid found in Coptidis Rhizoma(goldenthread) extract, has multiple pharmacological effects such as anti-inflammatory, antimicrobial and anti-ischemic effects. In the present study, we examined the effects of berberine on neuronal survival and differentiation in a hippocampal precursor cell line and in the memory deficient rat model. Berberine increased in a dose dependent manner the survival of hippocampal precursor cells as well as differentiated cells. In addition, berberine promoted neuronal differentiation of hippocampal precursor cells. In the memory deficient rat model induced by stereotaxic injection of ibotenic acid into entorhinal cortex(Ibo model), hippocampal cells were increased about 2.7 fold in the pyramidal layer of CA1 region and about 2 fold in the dentate gyrus by administration of berberine after 2 weeks of ibotenic acid injection. Furthermore, neuronal cells immunoreactive to calbindin were increased in the hippocampus and entorhinal cortex area by administration of berberine. Taken together, these results suggest that berberine has neuroprotective effect in the Ibo model rat brain by promoting the neuronal survival and differentiation.

• Journal of Haehwa Medicine
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• v.25 no.1
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• pp.37-44
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• 2016

Objectives : This study was designed to investigate the effect of Gamishinchubogun-tang (JiaweiShenzhuibujian-tang; GSB) on regeneration of PC12 cells. Methods : PC12 cells have been used extensively as a model for studying the cellular and molecular effects of neuronal cells. In order to check the effect of GSB on the regeneration of PC12 cells, the morphological change of PC12 cells were observed comparatively in GSB group and control group. Results : The significant changes in neurite length of PC12 cells have been observed on GSB group. In proportion to the concentration of GSB it was observed an increase in neurite outgrowth. Conclusions : This study confirmed that GSB made a significant influence on regeneration of PC12 cells.

• Molecules and Cells
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• v.40 no.1
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• pp.10-16
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• 2017

When peripheral axons are damaged, neuronal injury signaling pathways induce transcriptional changes that support axon regeneration and consequent functional recovery. The recent development of bioinformatics techniques has allowed for the identification of many of the regeneration-associated genes that are regulated by neural injury, yet it remains unclear how global changes in transcriptome are coordinated. In this article, we review recent studies on the epigenetic mechanisms orchestrating changes in gene expression in response to nerve injury. We highlight the importance of epigenetic mechanisms in discriminating efficient axon regeneration in the peripheral nervous system and very limited axon regrowth in the central nervous system and discuss the therapeutic potential of targeting epigenetic regulators to improve neural recovery.