• YAKHAK HOEJI
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• v.40 no.6
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• pp.720-726
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• 1996

The neurotoxicity induced by L-glutamate in primary cultures of rat cortical cells could be attenuated by diterpene constituents of Ginkgo biloba leaves, ginkgolides A, B and C. At the concentration of 100 nM, ginkgolides up-regulated the activity of glutathione reductase in primary cultures of rat cortical cells exposed to 100 ${\mu}$M glutamate. Furthermore, ginkgolides increased the content of reduced glutathione in glutamate-treated cortical cells. However, ginkgolides showed little effect in reducing superoxide dismutase activity. Ginkgolides did, however, markedly block the production of malondialdehyde, a byproduct of lipid peroxidation in glutamate-treated rat cortical cells.

• YAKHAK HOEJI
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• v.41 no.1
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• pp.111-116
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• 1997

The neurotoxicity induced by L-glutamate in primary cultures of rat cortical cells could be attenuated by sesquiterpene constituent of Ginkgo biloba leaves, bilobalide. At the c oncentration of 100 nM, Bilobalide elevated the combined levels of reduced/oxidized glutathione in rat cortical cells exposed to 100 ${\mu}$M glutamate. Furthermore, bilobalide promoted a reduction in superoxide dismutase activity in glutamate-treated cells. Finally, bilobalide markedly inhibited the production of malondialdehyde. a measure of lipid peroxidation, in glutamate-treated rat cortical cells.

• YAKHAK HOEJI
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• v.39 no.4
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• pp.444-449
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• 1995

Primary cultures of rat cortical and chicken embryonic brain cells were employed to establish a reliable screening method for natural products blocldng or enhancing glutamate-induced neurotoxicity. Exposure of primary cultured rat cortical cells or chicken embryonic brain cells to high dose of glutamate resulted in the fragmentation of neutites and consequent neuronal death. The level of cytoplasmic lactate dehydrogenase(LDH), indicator for cell survival in cultures, was significantly reduced at exposure to glutamate. For the practical application of the methods, series of concentrations of plants extracts and positive control were applied prior to the glutamate insult on primary cultures of rat cortical and chicken embryonic, brain cells. Relative LDH level in cells was measured for the estimation of the effect of the test materials on the glutamatergic neurons. The validity of the present screening method for natural products acting on glutamatergic neurons was examined with dextromethorphan, a known glutamatergic antagonist. The treatment of 100 $\mu{M}$ dextromethorphan prevented the reduction of LDH in rat cortical and chicken embryonic brain cells caused by glutamate insult keeping 60% and 90% of LDH level in normal control, respectively. Above results indicate that primary cultures of rat cortical and chicken embryonic brain cells could be proper systems for the screening of potential natural agents acting on glutamatergic, neurons. Between the two types of cultures, primary culture of chicken embryonic brain cells seemed to be a better system for the primary screening, since it is technically easier and economical compared to that of rat cortical cells.

• The Journal of Korean Medicine
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• v.23 no.1
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• pp.120-132
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• 2002

Objectives : The purpose of this investigation was to evaluate the effect of Goomicheongsim-won Extracts on E20 corticells and P7 cerebellar cells exposed to hypoxia, and the effect on neuronal protection by elimination of Rhinoceros unicornis L. and/or Orpiment $As_2S_3$. Methods : P7 cerebellar cells were grown in various concentrations of KM-A, KM-B, KM- C and KM-D. On 7 DIV (day in vitro), cells were exposed to hypoxia (98% $N_2/5%{;}CO_2,{\;}3{\;}hr,{\;}37^{\circ}C$) and normoxia, and then further incubated for 3 days. Neuronal viabilities were expressed as percentages of control. E20 cortical cells were grown in various concentrations of KM-A, KM-B, KM-C, and KM-D. On 7 DIV, cells were exposed to hypoxia and normoxia, and then further incubated for 3 and 7 days. Results : I. The effect of KM-A on neuronal protection was significantly increased P7 cerebellar granule cells and E20 cortical cells on normoxia and hypoxia. 2. The effect of KM-B on neuronal protection was increased P7 cerebellar granule cells on normoxia, but was significantly decreased P7 cerebellar granule cells on hypoxia. The effect of KM-B on neuronal protection was non-significantly increased E20 cortical cells on normoxia and hypoxia. 3. The effect of KM-C on neuronal protection was non-significantly increased P7 cerebellar granule cells on normoxia and hypoxia and was decreased (p=0.058) on hyperconcentration of the extracts in normoxia. The effect of KM-C on neuronal protection was significantly increased P7 cerebellar granule cells and E20 cortical cells on normoxia and hypoxia (10 DIV), and the effect was E20 cortical cells on normoxia (14 DIV), non-significantly increased E20 cortical cells on hypoxia (14DIV). 4. The effect of KM-D on neuronal protection was increased P7 cerebellar granule cells on normoxia but was not on hyperconcentration of the extracts, was significantly decreased on hyperconcentration of the extracts in hypoxia. The effect of KM-D on neuronal protection was significantly increased E20 cortical cells on normoxia and was significantly increased E20 cortical cells increased on hypoxia (10 DIV). Conclusions : Goomicheongsim-won extracts had applicable effect on E20 corticells and P7 cerebellar cells exposed to hypoxia. The effect on neuronal protection by elimination of Rhinoceros unicornis L. and/or Orpiment $As_2S_3$ was changed.

• Journal of Korean Neurosurgical Society
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• v.41 no.6
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• pp.397-402
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• 2007

Objective : Balloon cells and dysplastic neurons are histopathological hallmarks of the cortical tubers of tuberous sclerosis complex [TSC] and focal cortical dysplasia [FCD] of the Taylor type. They are believed to be the epileptogenic substrate and cause therapeutic drug resistant epilepsy in man. P-glycoprotein [P-gp] is the product of multidrug resistance gene [MDR1], and it maintains intracellular drug concentration at a relatively low level. The authors investigated expression of P-gp in balloon cells and dysplastic neurons of cortical tubers in patients with TSC. Methods : An immunohistochemical study using the primary antibody for P-gp, as an indicative of drug resistance, was performed in the cortical tuber tissues in two patients of surgical resection for epilepsy and six autopsy cases. Results : Balloon cells of each lesion showed different intensity and number in P-gp immunopositivity. P-gp immunopositivity in balloon cells were 28.2%, and dysplastic neurons were 22.7%. These immunoreactivities were more prominent in balloon cells distributed in the subpial region than deeper region of the cortical tubers. Capillary endothelial cells within the cortical tubers also showed P-gp immunopositivity. Conclusion : In this study, the drug resistance protein P-glycoprotein in balloon cells and dysplastic neurons might explain medically refractory epilepsy in TSC.

• Natural Product Sciences
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• v.15 no.3
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• pp.125-129
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• 2009

Neurodegenerative diseases such as Alzheimer's disease, stroke, and Parkinson's disease, are caused by neuronal cell death. Apoptosis, oxidative stress, inflammation, excitotoxicity or ischemia are discussed to play a role of neuronal cell death. In order to find the candidate of neuroprotective agent, neuroprotective activity of some medicinal plants was investigated with in vitro assay system using glutamate-induced neurotoxicity in primary cultures of rat cortical cells. The aqueous methanolic extracts of twenty-seven medicinal plants were evaluated the protective effects against glutamate-injured excitotoxicity in rat cortical cells at the concentration of 50 $\mu$g/ml and 100 $\mu$g/ml, respectively. Among them, extracts of Lonicera japonica, Taraxacum platycarpum, Polygonum aviculare, Gardenia jasminoides, Forsythia viridissima, Lygodium japonicum, Panax notoginseng, Akebia quinata, Anemarrhena asphodeloides and Phellodendron amurense showed significantly neuroprotective activities against glutamate-induced neurotoxicity in primary rat cortical cells.

• Journal of Sericultural and Entomological Science
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• v.40 no.2
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• pp.91-96
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• 1998

In relation to cold acclimation, this experiment was carried out to understand the changes of the cortical cells in the living barks of the mulberry during wintering period. The living barks of three mulberry varieties(Kaeryangppong, Shinilppong and Yongcheonppong) were sampled from December, 1995 to March, 1996. The result of this experiment was summarized as follows. The cortical cells in the living barks of the mulberry in December were filled with small vacuoles. Plastids and mitochondrias were located near the nucleus. At this time, almost all starch granules disappeared from the plastids. In January and February, mitochondria, palstids and microbodys of the cortical cell were observed. As increasing temperature from March, dictysomes and polysomes were sparse. Again, starch granules disappeared were observed in the plastids. From the above result. starch granules in plastide of the cortical cell of the mulberry disappeared during cold acclimation stage. After late January, Proplastid was observed in the cortical cell and the ultrastructures of cortical cell were actively changed.

• Biomedical Science Letters
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• v.8 no.4
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• pp.251-256
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• 2002

This study was undertaken to determine the underlying mechanisms of reactive oxygen species-induced cell injury in renal epithelial cells and whether there is a difference in the role of lipid peroxidation between freshly isolated renal cells and cultured renal cells. Rabbit renal cortical slices were used as a model of freshly isolated cells and opossum kidney (OK) cells as a model of cultured cells. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release in renal cortical slices and frypan blue exclusion in OK cells. $H_2O$$_2$ was used as a drug model of reactive oxygen species. $H_2O$$_2$ induced cell injury in a dose-dependent manner in both cell types. However, renal cortical slices were resistant to $H_2O$$_2$ approximately 50-fold than OK cells. $H_2O$$_2$-induced cell injury was prevented by thiols (glutathione and dithiothreitol) and iron chelators (deferoxamine and phenanthroline) in both cell types. $H_2O$$_2$-induced cell injury in renal cortical slices was completely prevented by antioxidants N,N-diphenyl-p -phenylenediamine and Trolox, but the cell injury was not affected by these antioxidants in OK cells. $H_2O$$_2$ increased lipid peroxidation in both cell types, which was completely inhibited by the antioxidants. These results suggest that $H_2O$$_2$ induces cell injury through a lipid peroxidation-dependent mechanism in freshly isolated renal cells, but via a mechanism independent of lipid peronidation in cultured cells.

• ALGAE
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• v.20 no.4
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• pp.315-324
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• 2005

Anatomical organization of Stoechospermum marginatum reveals small cortical cells with moderately dense cytoplasm, overlying a multilayered medulla comparatively poor in cytoplasmic contents. The anticlinal walls of cortical cells show local thickenings rich in alginic acids. Sori form on both thallus surfaces and show tetrasporangia, paraphyses and sterile-cells. The unicellular paraphyses are rich in sulphated polysaccharides whereas multicellular ones have abundance of not only polysaccharides, but also of vacuoles and phenols. The sterile-cells are modified cortical cells present on either side of the tetrasporangium and bear cytoplasmic strands towards soral cavity. Various stages of tetrasporogenesis are seen in a single sorus. The developing tetrasporangium shows a two layered wall, where the outer one is rich in alginic acid and inner has sulphated polysaccharides. An apical pad aids tetraspore release. Also involved in the release process are sterile-cells, paraphyses and polysaccharides.

• Natural Product Sciences
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• v.14 no.3
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• pp.156-160
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• 2008

The methanolic extract of Rhus verniciflua Stokes (RVS-T) and its fractions (RVS-H, RVS-C, RVS-E and RVS-B) showed significant neuroprotective activity against glutamate-induced toxicity in primary cultures of rat cortical cells. RVS-B, which showed the most potent neuroprotective activity, was further fractionated to yield RVS-B5. Treatment of cortical cells with the RVS-T, RVS-B and RVS-B5 reduced the cellular ROS level and restored the reduced activities of glutathione reductase and SOD induced by glutamate. Although, the activity of glutathione peroxidase was not virtually changed by glutamate, RVS-B5 increased the glutathione peroxidase activity. In addition, these three tested fractions significantly restored the content of GSH which was decreased by glutamate insult in our cultures. Taken together, it could be postulated that RVS extract, in particular its fraction RVS-B5, protected neuronal cells against glutamate-induced neurotoxicity through acting on the antioxidative defense system.