• YAKHAK HOEJI
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• v.43 no.4
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• pp.535-540
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• 1999

Glutamate (Glu) receptor-mediated excitoxicity has been implicated in many acute and chronic types of neurological disorders. Exposure of mature rat cortical neurons (15-18 days in culture) to the various concentrations of Glu resulted in a marked neuronal death, whereas immature rat cortical neurons (4∼5 days in culture) were resistant to the Glu-induced toxicity. Glu receptor subtype-specific agonists showed differential extent of toxicity in the immature neurons. The neurons treated with NMDA or kainate (KA) did not exhibit damage. However, quisqualate (QA) treatment induced a considerable cell death (36.1%) in immature enurons. The non-NMDA antagonist DNQX did not reduce this response. Interestingly, the QA-induced toxicity was potentiated by spermine in a concentration-dependent manner. Again, the spermine-enhanced damage was not altered by the polyamine antagonist ifenprodil. Taken together, unlike NMDA or KA, QA can induce neurotoxicity in immature rat cortical neurons and the QA-induced toxicity was potentiated by spermine. The lack of antagonizing effects of DNQX and ifenprodil on QA-induced toxicity and the potentiated toxicity by spermine, respectively, implies that both QA receptor and the polyamine site of NMDA receptor may not mediate the neurotoxicity observed in this study, and that a distinct mechanism(s) may be involved in excitotoxicity in immature neurons.

• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.169-175
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• 1996

The reactivity of the sulfhydryl (thiol) group of homocysteine has been associated with an Increased risk of atherosclerosis, thrombosis and stroke. Thiols also react with nitric oxide (NO, an endothelium-derived relaxing factor (EDRF) ), forming S-nitrosothiols that have been reported to have potent vasodilatory and antiplatelet effects and been expected to decrease adverse vascular effects of homocysteine. The present study was aimed to Investigate whether the S-nitrosation of homocysteine modulates the neurotoxic effects of homocysteine. An 18 hour-exposure of cultured rat cortical neurons to homocysteine ( >1 mM) resulted in a significant neuronal cell death. At comparable concentrations ( <10 mM), however, S-nitrosohomocysteine did not induce neuronal cell death. Furthermore, S-nitrosohomocysteirle partially blocked NMDA-mediated neurotoxicity. S-nitrosohomocysteine also decreased NMDA-mediated increases in intracellular calcium concentration. The present data indicate that in brain nitric oxide produced from neuronal and nonneuronal cells can modulate the potential, adverse properties of homocysteine.

• The Journal of Korea Institute of Information, Electronics, and Communication Technology
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• v.3 no.4
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• pp.10-15
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• 2010

Cortical bone is composed of an osteon, which is a subunit of the cortical bone. At the center of the osteon, Haversian is located and it consists of blood vessels and nerves. Osteon is known to be inclined 5 to 15 degrees with respect to the long axis of a cortical bone, but the reason why it is inclined is not clear. Using the poroelastic calculation provides the pore pressure varies at the lacunar-canalicular network from -200KPa to 200KPa. This estimation is close to the result shown in the previous literature and it helps further cell culture experiment for elucidating the bone remodeling process.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.145-163
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• 2002

Objectives: The purpose of this investigation was to evaluate the effects of Woohwangcheongsim-won and to study the mechanism for neuronal death protection in hypoxia with Embryonic day 20 (E20) cortical cells of a rat (Sprague Dawley). Methods: E20 cortical cells were dissociated in neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Woohwangcheongsim-won was added to the culture media for 24 hrs or 72 hrs. On 17 DIV, cells were given a hypoxic shock and further incubated in normoxia for another three days. On 20 DIV, Woohwangcheongsim-won's effects for neuronal death protection were evaluated by LDH assay, propidium iodide stain and phospho-H2AX immunostain and the mechanisms were studied by Bcl-2, Bak, Bax, caspase family, PKCα, ca1pain I. Results & Conclusions : 1. This study indicated that Woohwangcheongsim-won's effects for neuronal death protection in hypoxia were confirmed by LDH assay, propidium iodide stain and phospho-H2AX immunostain in culture method of Embryonic day 20(E20) cortical neuroblasts. 2. Woohwangcheongsim-won's mechanisms for neuronal death protection in hypoxia are to reduce the membrane damage fraction, to restrain DNA truncate, to restrain inflow of cytochrome c into cellularity caused by Bak diminution, to reduce the caspase cascade intiator caspase-8 and the effector caspase-3, to reduce the calpain I activity and to increase PKCand its activity in the membrane fraction. (J Korean Oriental Moo 2002;23(3):145～163)

• The Journal of Korean Medicine
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• v.23 no.4
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• pp.125-139
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• 2002

Objectives: The purpose of this investigation is to evaluate the effects of Woohwangcheongsim-won and to study the mechanism for neuronal death protection in OGD (oxygen-glucose deprivation) model with embryonic day 20 (E20) cortical cells of a rat (Sprague Dawley). Methods: E20 cortical cells were dissociated in neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Woohwangcheongsim-won was added to the culture media for 72 hrs. On 17 DIV, cells were given an oxygen-glucose deprivation shock (2hrs and 4hrs) and further incubated in normoxia for another three days. On 20 DIV, Woohwangcheongsim-won's effects for neuronal death protection were evaluated by LDH assay and the mechanisms were studied by Bcl-2, Bak, Bax, caspase family. Results & Conclusions: 1. This study indicates that Woohwangcheongsim-won's effects for neuronal death protection in OGD model is confirmed by LDH assay in culture method of embryonic day 20(E20) cortical neuroblasts. 2. Woohwangcheongsim-won's mechanisms for neuronal death protection in OGD model are to restrain inflow of cytochrome c into cellularity caused by Bcl-2 increase (2hrs and 4hrs), to reduce the caspase cascade initiator caspase-8 (4hrs).

• 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.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.12-20
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• 1998

Primary neuronal culture was studied for observing effect of ginsenoside Rgl (Rgl) on serum-free medium induced apoptosis. Results showed that Rgl at concentration of 1 umol$.$ L-1 and 10 umol$.$L-1 could inhibit apoptosis, decrease intracellular calcium concentration in cultured cortical neurons, enhance SOD activity in both aged rat cortex and cultured cortical neurons, scavenge cytotoxic oxygen free radicals, decrease NO content and NOS activity in aged rat cortex and cultured cortical neurons, increase bel-2 gene expression in rat brain. These results provided new data for elucidating the anti-aging effect of Rgi. Rgl is considered to be a useful drug for treatment of Alzheimer's disease and brain aging.

• Childhood Kidney Diseases
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• v.20 no.2
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• pp.57-62
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• 2016

Purpose: We used technetium-99m dimercaptosuccinic acid (DMSA) scintigraphy to identify factors predictive of renal cortical defects in infants <3 months of age with urinary tract infections (UTIs). Methods: We retrospectively reviewed data on infants <3 months of age with culture-proven UTIs treated at a single center from March 2010 to February 2016. Blood samples were obtained for laboratory evaluation prior to commencement of antibiotic therapy. The therapeutic delay time (TDT) and therapeutic response time (TRT) were recorded. All patients were divided into two groups depending on features of their DMSA scans. We compared the demographic, clinical, and laboratory characteristics of the two groups. Results: A total of 119 infants (94 males and 25 females; mean age, $56.9{\pm}21.3days$) were included. Cortical defects were evident in the DMSA scans of 47 cases (39.5%). In infants with such defects, the peak temperatures ($38.9{\pm}0.57^{\circ}C$ vs. $38.4{\pm}0.81^{\circ}C$, P=0.001), the absolute neutrophil counts ($8,920{\pm}4,460/mm$ vs. $7,290{\pm}4,090/mm$, P=0.043), and the C-reactive protein (CRP) levels ($6.49{\pm}4.33mg/dL$ vs. $3.21{\pm}2.81mg/dL$, P=0.001) were significantly higher than those in infants without cortical defects. The TDT was also longer in those with cortical defects (P=0.037). Conclusion: We found that a TDT ${\geq}8.5hr$ (odds ratio [OR] 5.81), a peak temperature ${\geq}38.3^{\circ}C$ (OR 6.19), and a CRP level ${\geq}4.96mg/dL$ (OR 7.26) predicted abnormal DMSA scan results in infants <3 months of age with UTIs.

• The Journal of Internal Korean Medicine
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• v.24 no.2
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• pp.348-357
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• 2003

Objectives : The purpose of this investigation is to evaluate the effects of Aucklandiae Radix Moschus(木香 麝香)and to study the mechanism for neuronal death protection in hypoxia with Embryonic day 20 (E20) cortical cells of a rat (Sprague Dawley). Methods : E20 cortical cells used in this investigation were dissociated in Neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Aucklandiae Radix Moschus(木香 麝香) was added to the culture media for 72 hrs. On 17 DIV, cells were given a hypoxic shock and further incubated in normoxia for another three days. On 20 DIV, Moschus(麝香)'s effects for neuronal death protection were evaluated by LDH assay and the mechanisms were studied by Bcl-2, Bak, Bax, caspase family. Results : This study indicate that Aucklandiae Radix(木香)'s effects for neuronal death protection in normoxia and Scutellariae Radix(麝香)'s effects for neuronal death protection in hypoxia were confirmed by LDH assay in culture method of Embryonic day 20(E20) cortical neuroblast. Moschus(麝香)'s mechanism for neuronal death protection in hypoxia is to increase the anti-apoptosis protein Bcl-2. Conclusions : It may be reasonable to propose that Moschus(麝香) protects delayed neuronal death in hypoxia by increasing Bcl-2, thereby reducing mitochondrial permeability transition(PT) pores, the cytochrome c channels.

• Archives of Pharmacal Research
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• v.17 no.5
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• pp.343-347
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• 1994

Effects of betaine on glutamate-induced neurotoxicity were examined on primary culturs of chicken embryonic brain cells and on rat cortical cultures. Betaine was found to attenuate glutamate-induced neurotoxicity both morphologically and biochemically. A 30 min exposure of chicken embryonic brain cells cultured for 12 days to 500 .mu.M glutamate produced wide-spread acute neuronal swelling and neurtic fragmentation. A 2-h pretreatment of cultured chicken embryonic brain cells with i mM betaine prior to a 30 min exposure to 500 , mu, M glutamate significantly raised the survival rate of neurons in the culture. When chicken embryonic brain cells were pretreated for 2 h with i mM betaine followed by exposure to 100 .mu.M glutamate for 42 h, lactate dehydrogenase levels within the cells remained at 62% of .mu.M untreated control values while glutamate-treated control fell to 0% lactate dehydrogenase. Betaine also exerted attenuating effects on N-methyl-D-asparte-, kainate-and quisqualate-induced neurotoxicity in a similar manner to that observed with glutamate. Similar neuroprotective effects of betaine with rat cortical cultures.