• The Journal of Korean Physical Therapy
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• v.25 no.5
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• pp.352-359
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• 2013

Purpose: For patients with CNS injury who are restricted in the use of public transportation, car driving means more than simple movements and is essential for their independent lives, such as participation in society and returning to jobs. Therefore, in order to enhance the quality of life of disabled persons, their high perception and necessity of driving rehabilitation are required. The purpose of this study is to determine the perception and necessity of driver rehabilitation in patients with CNS injury. Methods: In order to survey the perception of patients with CNS injury and necessity of driving rehabilitation, questionnaires were distributed to patients with CNS injury. Questionnaires were composed of demographic characteristics, disability related characteristics, and driver's license related characteristics. Results: Our results showed that the number of driving participants with a driver's license for the disabled was significantly higher than that for non- driving participants with a previous general driver's license in the perception of driving rehabilitation. Conclusion: We suggest that driving rehabilitation for patients with CNS injury should be supported in terms of evaluation and treatment.

• Journal of Pharmacopuncture
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• v.12 no.1
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• pp.67-76
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• 2009

Objective : Following central nervous system(CNS) injury, inhibitory influences at the site of axonal damage occur. Glial cells become reactive and form a glial scar, gliosis. Also myelin debris such as MAG inhibits axonal regeneration. Astrocyte-rich gliosis relates with up-regulation of GFAP and CD81, and eventually becomes physical and mechanical barrier to axonal regeneration. MAG is one of several endogenous axon regeneration inhibitors that limit recovery from CNS injury and disease. It was reported that molecules that block such inhibitors enhanced axon regeneration and functional recovery. Recently it was reported that treatment with anti-CD81 antibodies enhanced functional recovery in the rat with spinal cord injury. So in this current study, the author investigated the effect of the water extract of Uncariae Ramulus et Uncus on the regulation of CD81, GFAP and MAG that increase when gliosis occurs. Methods : MTT assay was performed to examine cell viability, and cell-based ELISA, western blot and PCR were used to detect the expression of CD81, GFAP and MAG. Then also immunohistochemistry was performed to confirm in vivo. Results : Water extract of Uncariae Ramulus et Uncus showed relatively high cell viability at the concentration of 0.05%, 0.1% and 0.5%. The expression of CD81, GFAP and MAG in astrocytes was decreased after the administration of Uncariae Ramulus et Uncus water extract. These results was confirmed in the brain sections following cortical stab injury by immunohistochemistry. Conclusion : The authors observed that Uncariae Ramulus et Uncus significantly down-regulates the expression of CD81, GFAP and MAG. These results suggest that Uncariae Ramulus et Uncus can be a candidate to regenerate CNS injury.

• The Journal of Korean Physical Therapy
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• v.11 no.3
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• pp.133-140
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• 1999

Why does the CNS not regenerate after injury? The failure of axonal regeneration in the CNS after injury is not due to an inherent inability of these neurons to regrowth axon. Recently, an inhibitory substrate effect of CNS has been discovered which could be directly invoked in the lack of regeneration. The failure of axon regrowth in the CNS is crucially influenced by the presence of neurtie growth inhibitor NI35/250 and possibly also by molecules such as myelin associated glycoprotein(MAG) and chondroitin sulphate proteoglycans(CSPGs). The application of the monoclonal antibody IN-1, which efficinetly neutralizes the N135/250 inhibitory molecules. This new finding has a strong impact on the development of, a new neuroscienctific research directed to stimulate axonal regeneration. In this review summarize the current knowledge on the factors and molecules involved in the regeneration failure.

• The Journal of Internal Korean Medicine
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• v.30 no.1
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• pp.24-35
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• 2009

Object : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis makes physical and mechanical barriers. If gliosis formation could be suppressed, irreversible axon damage would be reduced. This could mean that an injured CNS could be regenerated. CD81 and GFAP have close relationships to gliosis. The increase in glial cells at CNS injury gives rise to the expression of CD81 and GFAP. CD81 was postulated to play a central role in the process of CNS scar formation. Method : In this study, the author investigated the effect of the water extract of the Moutan Radicis Cortex on regulation of CD81 and GFAP expression in injured CNS cells. MTT assay was used to examine cell viability, while RT-PCR and ELISA methods were carried out to measure the expression of CD81 and GFAP in the astrocyte. Results : We observed that water extract of the Moutan Radicis Cortex increased cell viability under hypoxia induced by $CoCl_2$ and suppressed the expression of CD81 and GFAP up-regulated by hypoxia. Conclusion : These results suggest that the Moutan Redicis Cortex could promote neural regeneration as a consequence of protecting CNS cells from hypoxia and suppressing the reactive gliosis following CNS injury.

• Science of Emotion and Sensibility
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• v.7 no.2
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• pp.179-186
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• 2004

Acute spinal cord injury can produce neurologic injury with many physical, psychological and social ramifications. It has been shown that two separate components combine to produce neurologic damage in acute spinal cord injury : the primary and secondary injuries. The primary mediators of spinal cord injury include the actual mechanical tissue disruption which is a passive process that occurs immediately following the trauma. A secondary injury cascade follows which appears mediated by cellular and molecular processes working through complex mechanisms. Both the primary and secondary injury cascades produce cell death both in neuronal and supporting cell tissues. Recovery from central nervous system(CNS) disorders is hindered by the limited ability of the vertebrate CNS to regenerate injured cells, replace damaged myelin sheath, and re-establish functional neuronal connections. Of many CNS disorders including multiple sclerosis, stroke, and other trauma, spinal cord injury is one of the important diseases because of the direct association with the functional loss of the body. Previous studies suggest that substantial recovery of function might be achieved through regeneration of lost neuronal cells and remyelination of intact axon in spinal cord injury which is occurred frequently. As a therapeutic approach in spinal cord injury, recently, cell transplantation provides a potential solution for the treatment of spinal cord injury. This review describes the characteristics of spinal cord injury and presents some evidence supporting functional recovery after cell transplantation following spinal cord injury.

• Journal of Oriental Neuropsychiatry
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• v.20 no.1
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• pp.177-197
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• 2009

Objectives : Gliosis disturbs recovery of damaged astrocytes following central nervous system(CNS) injury. Gliosis relates to up-regulation of CD81 and GFAP. In glial cells at injured CNS, the expression of CD81 and GFAP is increased. It is possible that when the gliosis formation is suppressed, regeneration of oxons can occur. According to the recent study, the treatment with anti CD81 antibodies enhanced functional recovery in rats with spinal injury. So, the author studies the effect of water extract of Radix Ginseng on regulation of CD81 and GFAP with CNS injury. Methods : In the cell study, hypoxic damage was induced by CoC12. And according to Longa et al, cerebral ischemia was made by middle cerebral artery occlusion in the rat. Cross sections of rat brain were examined under microscope. MTT analysis was performed to examine cell viability, cell based ELISA, Western Blot and PCR were used to detect the expression of CD81 and GFAP. Results : The following results were obtained. 1. We found that CD81 and GFAP were decreased in hypoxic injured cells following Radix Ginseng administration. 2. We injected the extract of Radix Ginseng to the middle cerebral artery occlusion in rats, and the immunohistochemistry analysis showed that CDS1 and GFAP were decreased. Conclusions : These results show that the extract of Radix Ginseng could suppress the gliosis formation and prevent cell death, by controlling the expression of CDS1 and GFAP. Therefore, Radix Ginseng could be a useful to regenerate CNS injury.

• BMB Reports
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• v.35 no.1
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• pp.94-105
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• 2002

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

• BMB Reports
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• v.41 no.8
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• pp.560-567
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• 2008

The importance of lipids in cell signaling and tissue physiology is demonstrated by the many CNS pathologies involving deregulated lipid metabolism. One such critical metabolic event is the activation of phospholipase $A_2$ ($PLA_2$), which results in the hydrolysis of membrane phospholipids and the release of free fatty acids, including arachidonic acid, a precursor for essential cell-signaling eicosanoids. Reactive oxygen species (ROS, a product of arachidonic acid metabolism) react with cellular lipids to generate lipid peroxides, which are degraded to reactive aldehydes (oxidized phospholipid, 4-hydroxynonenal, and acrolein) that bind covalently to proteins, thereby altering their function and inducing cellular damage. Dissecting the contribution of $PLA_2$ to lipid peroxidation in CNS injury and disorders is a challenging proposition due to the multiple forms of $PLA_2$, the diverse sources of ROS, and the lack of specific $PLA_2$ inhibitors. In this review, we summarize the role of $PLA_2$ in CNS pathologies, including stroke, spinal cord injury, Alzheimer's, Parkinson's, Multiple sclerosis-Experimental autoimmune encephalomyelitis and Wallerian degeneration.

• Biomolecules & Therapeutics
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• v.28 no.1
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• pp.45-57
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• 2020

In the neurovascular unit, the neuronal and vascular systems communicate with each other. O₂ and nutrients, reaching endothelial cells (ECs) through the blood stream, spread into neighboring cells, such as neural stem cells, and neurons. The proper function of neural circuits in adults requires sufficient O₂ and glucose for their metabolic demands through angiogenesis. In a central nervous system (CNS) injury, such as glioma, Parkinson's disease, and Alzheimer's disease, damaged ECs can contribute to tissue hypoxia and to the consequent disruption of neuronal functions and accelerated neurodegeneration. This review discusses the current evidence regarding the contribution of oxygen deprivation to CNS injury, with an emphasis on hypoxia-inducible factor (HIF)-mediated pathways and Notch signaling. Additionally, it focuses on adult neurological functions and angiogenesis, as well as pathological conditions in the CNS. Furthermore, the functional interplay between HIFs and Notch is demonstrated in pathophysiological conditions.

• Journal of Acupuncture Research
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• v.24 no.6
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• pp.137-148
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• 2007

Objectives : Following central nervous system (CNS) injury, inhibitory influences at the site of axonal damage occur. Glial cells become reactive and form a glial scar, know as gliosis. As well,myelin debris such as MAG inhibits axonal regeneration. Astrocyte-rich gliosis relates to up-regulation of GFAP and CD81, and eventually becomes a physical and mechanical barrier to axonal regeneration. It is postulated that when the astrocytic reaction is absent, regeneration of axons can occur. It was reported that treatment with anti CD81 antibodies enhanced functional recovery in rats with spinal cord injury. Methods : MAG is one of several endogenous axon regeneration inhibitors that limit recovery from central nervous system injury and disease. It was reported that molecules which block such inhibitors enhanced axon regeneration and functional recovery. Results : In this current study, the author investigated the effect of the water extract of Ginseng Radix on the regulation of CD81, GFAP and MAG which increases when gliosis occurs. MTT analysis was performed to examine cell viability, and cell based ELISA, Western Blot and PCR were used to detect the expression of CD81, GFAP and MAG. Immunohistochemistry was also performed to confirm in vivo. Conclusions : We observed that Ginseng Radix significantly down-regulates the expression of CD81, GFAP and MAG by means of cell based ELISA, Western Blot and PCR. In immunohistochemistry, expression of CD81, GFAP and MAG also decreased. Taken together, these results suggest that Ginseng Radix can be a candidate for regenerating CNS injury.