• 한방안이비인후피부과학회지
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• 제29권3호
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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.

• Biomolecules & Therapeutics
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• 제28권6호
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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.

• 한국수정란이식학회:학술대회논문집
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• 한국수정란이식학회 2003년도 제3회 발생공학 국제심포지움 및 학술대회
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• pp.69-69
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• 2003

• The Korean Journal of Physiology and Pharmacology
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• 제10권3호
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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.

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 2007년도 춘계 학술대회
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• pp.16-16
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• 2007

• 한국발생생물학회:학술대회논문집
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• 한국발생생물학회 2005년도 제5회 발생공학 국제심포지엄 및 학술대회
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• pp.64-65
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• 2005

• 한국수정란이식학회:학술대회논문집
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• 한국수정란이식학회 2005년도 제5회 발생공학 국제심포지엄 및 학술대회
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• pp.64-65
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• 2005

• The Korean Journal of Physiology and Pharmacology
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• 제10권3호
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• pp.111-121
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• 2006

Neuroprotective properties of lithium were evaluated by using in vivo NMDA excitotoxicity model. Systemic injection of NMDA to young mice induced neuronal apoptosis mediated by both TNFR-l and Fas ligand, and long-term lithium treatment showed noticeable neuroprotection against NMDA-induced excitotoxicity: NMDA-damaged neurons expressed several apoptosis-related gene products such as TNFR-l, Fas ligand, and caspase-3, and these gene expressions were not found in the brain of mice chronically treated with lithium. Therefore, it is highly likely that the protection offered by chronic lithium treatment occurred at far upstream of caspase activation, since the chronic lithium treatment increased the expression of Bcl-2, an important antiapoptotic gene known to act upstream of caspase cascade. Timm's histochemistry indicated the complete blockade of the NMDA insults by the treatment. There was no indication of axonal regeneration, which follows synaptic degeneration induced by neuronal damage. Furthermore, this study reports for the first time that TNFR-l and Fas ligand are involved in neuroprotective effects of lithium in NMDA-induced neuronal apoptosis.

• 약학회지
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• 제44권6호
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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.

• The Korean Journal of Physiology and Pharmacology
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• 제5권5호
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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.