• The Journal of Korean Physical Therapy
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• v.9 no.1
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• pp.117-126
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• 1997

This Study was carried out to investigate the secondary cental nuclei innervating rat parotid gland. PRV-BaBlu as a neuronal tracer was injected into the left parotid gland and brains obtained through cardiac perfusion were treated by immunohistochemical staining. The results were as follows: L. The secondary central nuclei innervating rat parotid gland were paraventricular nucleus and central part of amygdaloid complex largely in diencephalon. 2. The paraventricular nucleus and central part of amygdaloid complex in diencephalon showed morphological asymmetry between PRV-BaBlu injected site and uninjected one. 3. The Ratio between total neurons and PRV-BaBlu infected neurons in paraventricular nucleus was $27.62{\pm}16.23\%$ in left and $12.78{\pm}8.69\%$ in right. 4. The Ratio between total neurons and PRV-BaBlu infected neurons in central part of amygdaloid nucleus was $14.25{\pm}9.26\%$ in left and $8.35{\pm}6.26\%$ in right.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.269-278
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• 2014

Various antiepileptic drugs (AEDs) especially enzyme-inducing AEDs might be associated with increased vascular risk, through impairment of the endogenous antioxidative ability which may trigger oxygen-dependent tissue injury. Lamotrigine (LTG) a non-enzyme-inducing AED has scarce information regarding its effects on oxidative stress. The present study aimed to study the possible modulation of vascular risk factors of epileptogenesis by LTG, in a rat model of kindling seizure induced by pentylenetetrazole (PTZ). Four groups of male Wister rats were used; vehicle control group, PTZ group (alternate day PTZ, 30 mg/kg, i.p), LTG/PTZ group (LTG 20 mg/kg/day p.o and alternate day PTZ) and LTG group. The study period was 5 weeks. Lipoproteins and total homocysteine (tHcy), malondialdehyde (MDA) and reduced glutathione (GSH) were measured. Aortic endothelial function study and histopathological examination of the rats' brains, aortas and coronaries were conducted. Serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C), tHcy, MDA, GSH levels were significantly higher in epileptic rats than normal controls rats. A decrease in HDL-cholesterol with high atherosclerotic index was also demonstrated. The administration of LTG improved the PTZ-kindled seizures. It produced a significant decrease in TC, TG and LDL-cholesterol, MDA, aortic GSH and increase in HDL-cholesterol with no significant effect on serum GSH and tHcy levels. LTG improved endothelium-dependent relaxation, decreased hippocampal neurodegenerative changes and atherosclerotic changes of aortas and coronaries. LTG decreased seizures severity, hippocampal damage and improved vascular risk markers in this rat model of kindling seizures.

• Journal of Life Science
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• v.9 no.6
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• pp.722-727
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• 1999

We carried out immunoblot analyses to study expression and subcellular distribution of the N-methyl-D-aspartate receptor(NR) subunits in salmon (Chum Salmon, Oncorhynchus keta). We prepared subcellular fractions such as brain homogenates, synaptosomes, and postsynaptic density (PSD) from salmon brains, and analyzed protein compositions by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). In a Coomassie-stained 6% SDS-gel, about 20 distinct major protein bands could be identified in the PSD fraction. Immunoblot analyses using antibodies against rat NR subunit 2A and 2B antigens (NR2A and NR2B, respectively) showed weak but evident signals at the 180 kDa positions in the salmon PSD fractions. However, in contrast to rat NRs, the salmon NR2A and NR2B are not recognized by a phosphotyrosine-specific antibody suggesting that the salmon NRs are regulated differently from those of the rat by protein tyrosine kinases. Our results indicate that NR2A and NR2B subunits are expressed in the salmon PSD fraction but not regulated by tyrosine phosphorylation.

• The Journal of Korean Medicine
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• v.32 no.5
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• pp.100-113
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• 2011

Objectives: Brain edema is brain swelling that occurs due to the accumulation of excess water in the brain parenchyma. AQP4 and AQP9 are water-channel proteins expressed strongly in the brain and control water fluxes into and out of the brain parenchyma. This study was conducted to evaluate effect of Hwangnyeonhaedok-tang on brain edema and intracerebral hemorrhage. Methods: Intracerebral hemorrhage was induced by intrastriatal injection of type IV collagenase(0.23 U/${\mu}l$, 0.1 ${\mu}l$/min) into Sprague-Dawley rat brains. Hwangnyeonhaedok-tang water extract(1,000 mg/kg) was administered orally three times every 20 hours from 4 hours after ICH operation. Then hematoma volume, brain edema percentage, and water content of brain tissue were measured. Immuno-histochemistry was performed for AQP4 and AQP9 expressions in the brain sections and area % of immuno-labeling was analyzed with image analyzing system. Results: 1. Water extract of Hwangnyeonhaedok-tang reduced hematoma volume of ICH induced rat. 2. Water extract of Hwangnyeonhaedok-tang reduced MPO positive neutrophils in the perihematoma of the ICH induced rat. 3. Water extract of Hwangnyeonhaedok-tang reduced brain edema percentage and water content of brain tissue of ICH induced rat. 4. Water extract of Hwangnyeonhaedok-tang reduced AQP4 immuno-positive cells in the perihematoma of the ICH induced rat. 5. Water extract of Hwangnyeonhaedok-tang reduced AQP9 immuno-positive cells in the perihematoma of the ICH induced rat. Conclusions: These results suggest that Hwangnyeonhaedok-tang decreases intracerebral hemorrhage and brain edema by means of downregulating AQP4 and AQP9 expressions in the brain.

• Journal of Sasang Constitutional Medicine
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• v.27 no.2
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• pp.270-287
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• 2015

Objectives To evaluate the neuroprotective effects of modified Yuldahanso-tang (MYH) in a Parkinson's disease mouse model. Methods 1) Four groups (each of 8 rats per group) were used in this study. 2) The neuroprotective effect of MYH was examined in a Parkinson's disease mouse model. C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg/day), intraperitoneal (i.p.) for 5 days. 3) The brains of 2 mice per group were removed and frozen at $-20^{\circ}C$, and the striatum-substantia nigra part was seperated. The protein volume was measured by Bradford method following Bio-Rad protein analyzing kit. Using mouse/Rat Dopamine ELISA Assay Kit. 4) The brains of 2 mice per group were separated and removed. TH-immunohistochemical was examined in the MPTP-induced Parkinson's disease mice to evaluate the neuroprotective effects of MYH on ST and SNpc. 5) Two mice out of each group were anesthetized and skulls were opened from occipital to frontal direction to take out the brains. The brains added TTC solution for 20 minutes for staining. 6) The water tank used for morris water maze test was filled with $28^{\circ}C$ water, and a round platform of 10cm in diameter was installed for mice to step on. The study was carried out once a day within 30 seconds, keep exercising to step on the platform in the pool. 7) The brains of two mice out of each group were fixed in 10% formaldehyde solution and paraphillin substance was infiltrated. They were fragmented by microtome, and observed under an optical microscope after Hematoxylin & Eosin staining. 8) A round acrylic cylinder with its upper side open was filled with clean water and depressive mouse models were forced to swim for 15 minutes. After 24 hours the animals were put in the same equipment for 5 minutes and were forced to swim. 9) The convenient, simple, and accurate high-performance liquid chromatography (HPLC) method was established for simultaneous determination of Neurotransmitters in MPTP-MYH group. Results 1) MYH possess Dopamine cell protective effect on MPTP-induced injury in striatum and substantia nigra pars compacta. 2) MYH inhibits the loss of tyrosine hydroxylase-immunoreacitive (TH-IR) cells in the striatum and substantia nigra pars compacta on MPTP-induced injury in C57BL/6 mice. 3) MYH possesses improvement effect on MPTP-induced memory deterioration in C57BL/6 mice through the reduction of prolongated Sort of lost time by MPTP injection using the Morris water maze test. 4) MYH possesses hippocampal neuron protective effect on MPTP-induced injury in C57BL/6 mice. 5) MYH possesses improvement effect on MPTP-induced motor behaviour deficits and depression in C57BL/6 mice through the reduction of prolongated losing motion by MPTP injection using the Forced swimming test. 6) MYH increases serotonin product amount on MPTP-induced injury in C57BL/6 mice. Conclusions This experiment suggests that the neuroprotective effect of MYH is mediated by the increase in Dopamin, TH-ir cell, Hippocampus and Serotonin. Furthermore, MYH essential oil may serve as a potential preventive or therapeutic agent regarding Parkinson's disease.

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.608-615
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• 2018

Benzalkonium chloride, diazolidinyl urea, and imidazolidinyl urea are commonly used preservatives in cosmetics. Recent reports suggested that these compounds may have cellular and systemic toxicity in high concentration. In addition, diazolidinyl urea and imidazolidinyl urea are known formaldehyde (FA) releasers, raising concerns for these cosmetic preservatives. In this study, we investigated the effects of benzalkonium chloride, diazolidinyl urea, and imidazolidinyl urea on ROS-dependent apoptosis of rat neural progenitor cells (NPCs) in vitro. Cells were isolated and cultured from embryonic day 14 rat cortices. Cultured cells were treated with 1-1,000 nM benzalkonium chloride, and $1-50{\mu}M$ diazolidinyl urea or imidazolidinyl urea at various time points to measure the reactive oxygen species (ROS). PI staining, MTT assay, and live-cell imaging were used for cell viability measurements. Western blot was carried out for cleaved caspase-3 and cleaved caspase-8 as apoptotic protein markers. In rat NPCs, ROS production and cleaved caspase-8 expression were increased while the cell viability was decreased in high concentrations of these substances. These results suggest that several cosmetic preservatives at high concentrations can induce neural toxicity in rat brains through ROS induction and apoptosis.

• Biomolecules & Therapeutics
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• v.23 no.6
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• pp.531-538
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• 2015

Preceding infection or inflammation such as bacterial meningitis has been associated with poor outcomes after stroke. Previously, we reported that intracorpus callosum microinjection of lipopolysaccharides (LPS) strongly accelerated the ischemia/reperfusionevoked brain tissue damage via recruiting inflammatory cells into the ischemic lesion. Simvastatin, 3-hydroxy-3-methylgultaryl (HMG)-CoA reductase inhibitor, has been shown to reduce inflammatory responses in vascular diseases. Thus, we investigated whether simvastatin could reduce the LPS-accelerated ischemic injury. Simvastatin (20 mg/kg) was orally administered to rats prior to cerebral ischemic insults (4 times at 72, 48, 25, and 1-h pre-ischemia). LPS was microinjected into rat corpus callosum 1 day before the ischemic injury. Treatment of simvastatin reduced the LPS-accelerated infarct size by 73%, and decreased the ischemia/reperfusion-induced expressions of pro-inflammatory mediators such as iNOS, COX-2 and IL-$1{\beta}$ in LPS-injected rat brains. However, simvastatin did not reduce the infiltration of microglial/macrophageal cells into the LPS-pretreated brain lesion. In vitro migration assay also showed that simvastatin did not inhibit the monocyte chemoattractant protein-1-evoked migration of microglial/macrophageal cells. Instead, simvastatin inhibited the nuclear translocation of NF-${\kappa}B$, a key signaling event in expressions of various proinflammatory mediators, by decreasing the degradation of $I{\kappa}B$. The present results indicate that simvastatin may be beneficial particularly to the accelerated cerebral ischemic injury under inflammatory or infectious conditions.

• Journal of electromagnetic engineering and science
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• v.15 no.3
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• pp.173-180
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• 2015

To explore the effects of radiofrequency electromagnetic field on the fate of neuronal cells, we investigated whether exposure to 915 MHz radiofrequency identification (RFID) caused morphological changes in neuronal cells in rat hippocampal dentate gyrus (DG). A reverberation chamber was used as a whole-body RFID exposure system. Rats were assigned to two groups: sham- and RFID-exposed groups. Rats in the RFID-exposed group were exposed to RFID at 4 W/kg specific absorption rate (SAR) for 8 hours daily, 5 days per week, for 2 weeks. Morphological evaluation of DG was performed using immunohistochemistry with doublecortin (DCX) as a neuronal precursor cell marker and neuronal nuclei (NeuN) as a mature neuronal cell marker. No significant morphological changes in DCX+ or NeuN+ cells in the DG of RFID-exposed rats were observed. These results suggest that RFID exposure induces no significant change in DCX+ neuronal precursor or NeuN+ neuronal cells in DG of rats.

• Biomolecules & Therapeutics
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• v.21 no.4
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• pp.313-322
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• 2013

Previous studies have demonstrated that repeated administration of the exogenous stress hormone corticosterone (CORT) induces dysregulation in the hypothalamic-pituitary-adrenal (HPA) axis and results in depression and anxiety. The current study sought to verify the impact of catechin (CTN) administration on chronic CORT-induced behavioral alterations using the forced swimming test (FST) and the elevated plus maze (EPM) test. Additionally, the effects of CTN on central noradrenergic systems were examined by observing changes in neuronal tyrosine hydroxylase (TH) immunoreactivity in rat brains. Male rats received 10, 20, or 40 mg/kg CTN (i.p.) 1 h prior to a daily injection of CORT for 21 consecutive days. The activation of the HPA axis in response to the repeated CORT injections was confirmed by measuring serum levels of CORT and the expression of corticotrophin-releasing factor (CRF) in the hypothalamus. Daily CTN administration significantly decreased immobility in the FST, increased open-arm exploration in the EPM test, and significantly blocked increases of TH expression in the locus coeruleus (LC). It also significantly enhanced the total number of line crossing in the open-field test (OFT), while individual differences in locomotor activities between experimental groups were not observed in the OFT. Taken together, these findings indicate that the administration of CTN prior to high-dose exogenous CORT significantly improves helpless behaviors, possibly by modulating the central noradrenergic system in rats. Therefore, CTN may be a useful agent for the treatment or alleviation of the complex symptoms associated with depression and anxiety disorders.

• Archives of Pharmacal Research
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• v.10 no.4
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• pp.212-218
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• 1987

Intact brain cell aggregates were dissociated from adult rat brains without cerebellum using a sieving technique. This proparation was used to elucidate the binding characteristics of agonist to muscarinic acetylcholine receptors (mAchR) in brain. Incubation of cells with carbamylcholine (carbachol) was shown agonist-induced receptor down-regulation depending on the concentration of agonist, not depending on the incubation time. This effect of carbachol was due to a reduction in the maximal binding capacity ($B_{max}$) to the mAchR without decreasing the affinity of the remaining receptors in incubation at 37.deg.C but was not apparent inincubation at $15^{\circ}}C$In addition, it was abolished when the receptors were blocked by atropine. The decline in ($^3H$)N-methylscopolamine (($^3H$)NMS) binding induced by agonist was reflected as a significant reduction in the receptor density with no change in receptor affinity, suggesting that 'true' receptor down-regulation takes place. Moreover, when the receptors were labeled with the lipophilic antagonist ($^3H$) quinuclidinyl benzilate (($^3H$) QNB) insted of the hydrophilic ligand ($^3H$)NMS, the magnitude of the observed receptor down-regulation was significantly lower in case of the former than the latter. This suggested that exposure of intact brain cells to muscarinic agonists might induce a slight degree of accumulation of receptors in intracellular sites before the receptors are actually degraded.