• Title, Summary, Keyword: Neuroprotection

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The Study on the Korean and Western Medical Literatures for Neuroprotection Therapy of Glaucoma (녹내장의 신경 보호 치료에 대한 동서의학적 고찰)

  • Jung, Hye-Jin;Ko, Woo-Shin;Yoon, Hwa-Jung
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.29 no.3
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    • pp.59-73
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    • 2016
  • Objectives : The aim of this study is to understand neuroprotection therapy of glaucoma with both Korean and western medicine.Methods :  We searched Pubmed on the title "glaucoma" and "neuroprotection" and also searched CNKI(China National Knowledge Infrastructure) and OASIS(Oriental Medicine Advanced Searching Integrated System) on the title "glaucoma".Results : The results are as follows. 1. In western medicine, excitotoxicity inhibition, immunomodulation, oxidative stress suppression, supplement of NTFs and stem cell therapy are studied with neuroprotection therapy of glaucoma. 2. Treatment of glaucoma in TCM and Korean medicine are associated with liver(肝) and kidney(腎).Conclusions : Korean medical approaches on neuroprotection therapy of glaucoma can be significant, and further studies are needed to research.

Inhibition of LPA5 Activity Provides Long-Term Neuroprotection in Mice with Brain Ischemic Stroke

  • Sapkota, Arjun;Park, Sung Jean;Choi, Ji Woong
    • Biomolecules & Therapeutics
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    • v.28 no.6
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    • pp.512-518
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    • 2020
  • Stroke is a leading cause of long-term disability in ischemic survivors who are suffering from motor, cognitive, and memory impairment. Previously, we have reported suppressing LPA5 activity with its specific antagonist can attenuate acute brain injuries after ischemic stroke. However, it is unclear whether suppressing LPA5 activity can also attenuate chronic brain injuries after ischemic stroke. Here, we explored whether effects of LPA5 antagonist, TCLPA5, could persist a longer time after brain ischemic stroke using a mouse model challenged with tMCAO. TCLPA5 was administered to mice every day for 3 days, starting from the time immediately after reperfusion. TCLPA5 administration improved neurological function up to 21 days after tMCAO challenge. It also reduced brain tissue loss and cell apoptosis in mice at 21 days after tMCAO challenge. Such long-term neuroprotection of TCLPA5 was associated with enhanced neurogenesis and angiogenesis in post-ischemic brain, along with upregulated expression levels of vascular endothelial growth factor. Collectively, results of the current study indicates that suppressing LPA5 activity can provide long-term neuroprotection to mice with brain ischemic stroke.

Estrogen Pretreatment of Organotypic Hippocampal Slices Protects Neurons against Oxygen-Glucose Deprivation with Akt Activation

  • Park, Eun-Mi;Park, Sung-Hui;Lee, Kyung-Eun
    • The Korean Journal of Physiology and Pharmacology
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    • v.10 no.3
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    • pp.123-129
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    • 2006
  • In several experimental models, estrogens protect neurons against ischemic insults. However, the recent clinical studies of hormone replacement showed negative results to prevent stroke. Therefore, optimal models to study estrogen replacement for neuroprotection are needed before its clinical ap-plication. Organotypic hippocampal slice under oxygen-glucose deprivation (OGD) has been established as a model of cerebral ischemia and has advantages to study drug effects. We investigated whether estrogen protected CAI neurons and affected activation of Akt (pAkt) in CAI region under OGD. Thus, rat hippocampal slices on day 7 of culture were treated with $17-{\beta}$ estradiol (E, 1 nM) for 7 days before 30 min OGD, and cell death of CAI neurons was quantified by propidium iodide (PI) staining and expression of pAkt was studied by Western blot and immunofluorescence. PI intensity in slices treated with E was significantly reduced 72 hour after OGD compared to that of non-treated slices (p < 0.05). E pretreatment also increased the expression of pAkt 72 hour after OGD compared to that of no treatment (p<0.01). These data suggest that estrogen pretreatment may rescue neurons from ischemic insults through the activation of Akt and also indicate that our model would be a useful alternative method to study the mechanisms and effects of estrogen replacement treatment for neuroprotection.

Neuroprotection in Schizophrenia and Its Therapeutic Implications

  • Kim, Yong-Ku;Na, Kyoung-Sae
    • Psychiatry investigation
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    • v.14 no.4
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    • pp.383-391
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    • 2017
  • Schizophrenia is a chronic and debilitating mental disorder. The persisting negative and cognitive symptoms that are unresponsive to pharmacotherapy reveal the impairment of neuroprotective aspects of schizophrenia. In this review, of the several neuroprotective factors, we mainly focused on neuroinflammation, neurogenesis, and oxidative stress. We conducted a narrative and selective review. Neuroinflammation is mainly mediated by pro-inflammatory cytokines and microglia. Unlike peripheral inflammatory responses, neuroinflammation has a role in various neuronal activities such as neurotransmission neurogenesis. The cross-talk between neuroinflammation and neurogenesis usually has beneficial effects in the CNS under physiological conditions. However, uncontrolled and chronic neuroinflammation exert detrimental effects such as neuronal loss, inhibited neurogenesis, and excessive oxidative stress. Neurogenesis is also a major component of neuroprotection. Adult neurogenesis mainly occurs in the hippocampal region, which has an important role in memory formation and processing. Impaired neurogenesis and an ineffective response to antipsychotics may be thought to indicate a deteriorating course of schizophrenia. Oxidative stress and excessive dopaminergic neurotransmission may create a vicious cycle and consequently disturb NMDA receptor-mediated glutamatergic neurotransmission. Based on the current evidences, several neuroprotective therapeutic approaches have been reported to be efficacious for improving psychopathology, but further longitudinal and large-sample based studies are needed.

Protective Effects of Opuntia Ficus-Indica and Saururus Chinensis on Free Radical-Induced Neuronal Injury in Mouse Cortical Cell Cultures (생쥐 피질세포배양에서 Free Radical 유발 신경손상에 대한 손바닥선인장 및 삼백초의 보호효과)

  • Wie, Myung-Bok
    • YAKHAK HOEJI
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    • v.44 no.6
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    • pp.613-619
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    • 2000
  • The author examined whether the methanol extracts of Opuntia ficus-indica fruit and Saururus chinensis have the inhibitory action on xanthine/xanthine oxidase (X/XO)-, $FeCl_2/ascorbic$ acid- and arachidonic acid-induced neurotoxicity in mouse cortical cell cultures. The methanol extracts ($10\;{\mu}g/ml{\sim}1\;mg/ml$) of Opuntia ficus-indica and Saururus chinensis were exhibited 53-89% and $48{\sim}100%$ inhibitory action on X/XO-induced neurotoxicity, respectively. At the range of same concentration, both extracts also attenuated the $FeCl_2/ascorbic$ acid-induced neurotoxicity by $35{\sim}100%$ and $15{\sim}98%$, respectively. In arachidonic acid neurotoxicity, the methanol extract (1 mg/ml) of Opuntia ficus-indica and Saururus chinensis reduced neuronal injury by 22% and 38%, respectively. These results suggest that Opuntia ficus-indica fruit and Saururus chinensis may contribute the neuroprotection in certain free radical-mediated neuronal injury.

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Neuroprotection of Lithium is Associated with Inhibition of Bax Expression and Caspase 8 Activation

  • Kwon, Gee-Youn;Kim, Soo-Kyung
    • The Korean Journal of Physiology and Pharmacology
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    • v.5 no.5
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    • pp.389-396
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    • 2001
  • Neuroprotective properties of lithium were investigated by using in vivo NMDA excitotoxicity model. The appearance of TUNEL positive cells was prominent within 24 h of NMDA (70 mg/kg, i.p.) injection in the regions of the cortex, hippocampal formation, and thalamus of mouse cerebrum. NMDA treatment resulted in the extensive enhancement of Bax immunoreactivity in the cortical and hippocampal regions. NMDA also increased the immunoreactivity of caspase 8 in the similar regions of the mouse cerebrum. However, the increased immunoreactivity of Bax and caspase 8 were dramatically attenuated by chronic lithium pretreatment (lithium chloride, 300 mg/kg/d, i.p. for $7{\sim}10$ days). At the same time, lithium ion blocked the appearance of TUNEL positive cells, and the morphological assessment indicated an effective neuroprotection by lithium against NMDA excitotoxicity. Although the exact action mechanism of lithium is not straightforward at this time, we propose that the inhibition of Bax and caspase cascade is involved in the neuroprotective action of lithium.

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