• Applied Microscopy
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• 제23권1호
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• pp.109-124
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• 1993

The prenatal development of thoracic spinal cord was studied by electron microscope in human embryos and fetuses ranging from 9mm to 260mm crown-rump length (5-30 weeks of gestational age). Ependymal cells in all fetal ages had conspicuous junctional complexes close to the lumen of the central canal into which microvilli and cilia projected. The ependymal cells contained numerous longitudinally arranged mitochondria, flattened cisternae of endoplasmic reticulum and Golgi complex. At 20 mm embryo, the floor and roof plates were composed of ependymoglial cells and undifferentiated neuroepithelial cells. The neuroepithelia of the sacral spinal cord were delineated from central medullary cord. By 100 mm fetus few undifferentiated neuroepithelial cells remained in the floor and roof plates. At 150 mm fetus, the whole central canal was formed by ciliated columnar epithelial cells containing cilia with basal bodies. The microvilli became tangled and club-shaped and formed a matted surface. The canal was filled with areas of dark and pale amorphous materials bounded by membrane-like structure. These two types of material were found throughout the whole central canal from 100 mm fetus onwards. By 260 mm fetus, microfibrils were first observed in the ependymal cells. In conclusion, it seems that early development and differentiation of central canal ependyma are simlar to that in other part of the brain ventricular system although ependymoglial cells are more prominent.

• Journal of Korean Neurosurgical Society
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• 제59권3호
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• pp.259-268
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• 2016

Objective : Accumulation of advanced glycation end-products (AGE) and mitochondrial glycation is importantly implicated in the pathological changes of the brain associated with diabetic complications, Alzheimer disease, and aging. The present study was undertaken to determine whether sildenafil, a type 5 phosphodiesterase type (PDE-5) inhibitor, has beneficial effect on neuronal cells challenged with AGE-induced oxidative stress to preserve their mitochondrial functional integrity. Methods : HT-22 hippocampal neuronal cells were exposed to AGE and changes in the mitochondrial functional parameters were determined. Pretreatment of cells with sildenafil effectively ameliorated these AGE-induced deterioration of mitochondrial functional integrity. Results : AGE-treated cells lost their mitochondrial functional integrity which was estimated by their MTT reduction ability and intracellular ATP concentration. These cells exhibited stimulated generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential, induction of mitochondrial permeability transition, and release of the cytochrome C, activation of the caspase-3 accompanied by apoptosis. Western blot analyses and qRT-PCR demonstrated that sildenafil increased the expression level of the heme oxygenase-1 (HO-1). CoPP and bilirubin, an inducer of HO-1 and a metabolic product of HO-1, respectively, provided a similar protective effects. On the contrary, the HO-1 inhibitor ZnPP IX blocked the effect of sildenafil. Transfection with HO-1 siRNA significantly reduced the protective effect of sildenafil on the loss of MTT reduction ability and MPT induction in AGE-treated cells. Conclusion : Taken together, our results suggested that sildenafil provides beneficial effect to protect the HT-22 hippocampal neuronal cells against AGE-induced deterioration of mitochondrial integrity, and upregulation of HO-1 is involved in the underlying mechanism.

• 한국연초학회지
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• 제19권2호
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• pp.136-144
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• 1997

Cigarette smoking is known to suppress both 1-methy14-phenyl-155,Ltetrahydropy-ridine (MPTP)-induced parkinsonism and idiopathic Parkinson's disease (PD). However, the precise mechanism underlying its protective action against PD is not clearly elucidated yet. In order to find possible clue on the mechanism of protective action of smoking, we investigated the inhibitory effect of cigarette smoke components on rat brain mitochondria1 monoamine oxidase B (MAO-B), responsible enzyme for the activation of MPTP to its toxic metabolitesr and identified the components having an inhibitory potency on this enzyme from cigarette smoke. Total 31 eligible constituents including nicotine were selected from cigarette smoke condensates via solvents partitioning and silica gel chromatographic separation, and inhibitory potencies of 19 components on MAO-B were determined. Hydroquinone and methylcatechol, the phenolic components, showed the strongest inhibitory potencies on MAO-B activity in the components tested. 3,4-Dihydroxybenzylamino, myosmine and indole in basic fracton, eugenol in phenolic fraction, and farnesol in neutral fraction also inhibited the enzyme activity dose-dependently. Among tobacco alkaloids tested only myosmine was effective for the inhibition of this enzyme. These results suggest that the decrease in MAO-B activity by such components derived from cigarette smoke seems to be related to the suppression of MPTP-induced neurotoxicity and to the less incidence of Parkinson's disease in smokers than in nonsmokers.

• 한국식품영양과학회지
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• 제13권4호
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• pp.459-468
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• 1984

The currently accepted model of membrane structure proposes a dynamic, asymmetric lipid matrix of phospholipids and cholesterol with globular proteins embedded across the membrane to various degrees. Most phospholipids are in the bilayer arrangement and also closely associated with integral membrane proteins or loosely associated with peripheral proteins. Biological functions of membrane, such as membrane-bound enzyme functions and transport systems, are influenced by the membrane physical properties, which are determined by fatty acid composition of phospholipids, polar head group composition and membrane cholesterol content. Polar and non-polar region of the phospholipid molecule can interact, with changes in the conformation of a membrane-associated protein altering either its catalytic activity or the protein's interaction with other membrane proteins. Mammalian dietary studies attempted to change the lipid composition of a few cell membranes have shown comparisons, using essential fatty acid-deficient diets. In recent years, Clandinin and a few other workers have pioneered the study proving the influence of dietary fat fed in a nutritionally complete diet on composition of phospholipid classes of cell membrane. Modulation caused by diet fat was rapid and reversible in phospholipid fatty acyl composition of membranes of cardiac mitochondria, liver cell, brain synaptosome and lymphocytes. These changes were at the same time, accompanied by variety of membrane associated functions controlled by membrane-bound enzymes, tranporter and receptor proteins. The findings suggest the basic concept of the necessity of dietary fatty acid balance if consistency of optimal membrane structural lipid composition is to be maintained, as well as the overall inadequacy of describing the nutritional-biochemical quality of a dietary fat solely by its content of linoleic acid. Furthermore, they give light on the possible application to clinical and preventive medicine.

• 한국수산과학회지
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• 제48권3호
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• pp.354-361
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• 2015

Mitochondrial heat shock protein 75 (mtHSP75) is a member of the HSP90 family and plays essential roles in refolding proteins of the mitochondrial matrix. Mitochondria provide energy in the form of ATP and generate reactive oxygen species (ROS). Heat shock proteins (HSPs) are activated in response to stress, and protect cells. In this study, we characterized the mtHSP75 of the big-belly seahorse Hippocampus abdominalis. The protein (BsmtHSP75) is encoded by an open reading frame (ORF) of 2,157 nucleotides, has 719 amino acids (aa), and is of molecular mass 82 kDa. BsmtHSP75 has two functional domains, a histidine kinase-like ATPase (HATPase_c) domain (123-276 aa) and an HSP90 family domain (302-718 aa). BsmtHSP75 was expressed in all tested tissues of healthy seahorses. The ovary contained the highest transcription level, followed (in order) by the blood, brain, and muscle. Pouch tissue showed the lowest expression level. The expression of BsmtHSP75 was significantly (P<0.05) up-regulated on viral or bacterial challenge, suggesting that BsmtHSP75 plays a role in the immune defense against bacterial and viral pathogens.

• The Korean Journal of Physiology and Pharmacology
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• 제16권6호
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• pp.423-429
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• 2012

Brain ischemia leads to overstimulation of N-methyl-D-aspartate (NMDA) receptors, referred as excitotoxicity, which mediates neuronal cell death. However, less attention has been paid to changes in synaptic activity and morphology that could have an important impact on cell function and survival following ischemic insult. In this study, we investigated the effects of reperfusion after oxygen/glucose deprivation (OGD) not only upon neuronal cell death, but also on ultrastructural and biochemical characteristics of postsynaptic density (PSD) protein, in the stratum lucidum of the CA3 area in organotypic hippocampal slice cultures. After OGD/reperfusion, neurons were found to be damaged; the organelles such as mitochondria, endoplasmic reticulum, dendrites, and synaptic terminals were swollen; and the PSD became thicker and irregular. Ethanolic phosphotungstic acid staining showed that the density of PSD was significantly decreased, and the thickness and length of the PSD were significantly increased in the OGD/reperfusion group compared to the control. The levels of PSD proteins, including PSD-95, NMDA receptor 1, NMDA receptor 2B, and calcium/calmodulin-dependent protein kinase II, were significantly decreased following OGD/reperfusion. These results suggest that OGD/reperfusion induces significant modifications to PSDs in the CA3 area of organotypic hippocampal slice cultures, both morphologically and biochemically, and this may contribute to neuronal cell death and synaptic dysfunction after OGD/reperfusion.

• The Korean Journal of Physiology and Pharmacology
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• 제23권2호
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• pp.121-130
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• 2019

Glutamate toxicity-mediated mitochondrial dysfunction and neuronal cell death are involved in the pathogenesis of several neurodegenerative diseases as well as acute brain ischemia/stroke. In this study, we investigated the neuroprotective mechanism of dieckol (DEK), one of the phlorotannins isolated from the marine brown alga Ecklonia cava, against glutamate toxicity. Primary cortical neurons ($100{\mu}M$, 24 h) and HT22 neurons (5 mM, 12 h) were stimulated with glutamate to induce glutamate toxic condition. The results demonstrated that DEK treatment significantly increased cell viability in a dose-dependent manner ($1-50{\mu}M$) and recovered morphological deterioration in glutamate-stimulated neurons. In addition, DEK strongly attenuated intracellular reactive oxygen species (ROS) levels, mitochondrial overload of $Ca^{2+}$ and ROS, mitochondrial membrane potential (${\Delta}{\Psi}_m$) disruption, adenine triphosphate depletion. DEK showed free radical scavenging activity in the cell-free system. Furthermore, DEK enhanced protein expression of heme oxygenase-1 (HO-1), an important anti-oxidant enzyme, via the nuclear translocation of nuclear factor-like 2 (Nrf2). Taken together, we conclude that DEK exerts neuroprotective activities against glutamate toxicity through its direct free radical scavenging property and the Nrf-2/HO-1 pathway activation.

• Journal of Medicine and Life Science
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• 제15권2호
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• pp.67-71
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• 2018

Neuronal excitotoxicity induces mitochondrial dysfunction and the release of proapoptotic proteins. Excitotoxicity, the process by which the overactivation of excitatory neurotransmitter receptors leads to neuronal cell death. Neuronal death by excitotoxicity was related to neuronal degenerative disorders and hypoxia, results from excessive exposure to excitatory neurotransmitters, such as glutamate. Glutamate acts at NMDA receptors in cultured neurons to increase the intracellular free calcium concentration. Therefore endogenous glutamate may be a key factor to regulate neuronal cell death via activating $Ca^{2+}$ signaling. For this issue, we tested some conditions to alter intracellular $Ca^{2+}$ level in dissociated hippocampal neurons of rats. Cultured hippocampal neuron were treated by KCl (20 mM), $CaCl_2$ (3.8 mM) and glutamate ($5{\mu}M$) for 24 hrs. Interestingly, The Optical Density of hippocampal neurons was increased by high KCl application in MTT assay data. This enhanced response by high KCl was dependent on synaptic $Ca^{2+}$ influx but not on intracellular $Ca^{2+}$ level. However, the number of neurons seemed to be not changed in Hoechst 33342 staining data. These results suggest that enhancement of synaptic activity plays a key role to increase mitochondrial signaling in hippocampal neurons.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2021년도 춘계학술대회
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• pp.57-57
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• 2021

Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. Stachys sieboldii Miq. (Chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of S. sieboldii Miq. (SSM) in OGD/R induced neuronal injury is not yet fully understood. The present research is aimed to investigate the protective effect and possible mechanisms of SSM extract treatment in an in vitro model of OGD/R to simulate ischemia/reperfusion Injury. Pretreatment of these cells with SSM significantly attenuated OGD/R-induced production of reactive oxygen species (ROS) by increasing GPx, SOD, and decreasing MDA. SSM decreased mitochondrial damage caused by OGD/R injury and inhibited the release of cyt-c from mitochondrion to cytoplasm in SH-SY5Y cells. Furthermore, neuronal cell apoptosis caused by OGD/R injury was inhibited by SSM, and SSM could decrease apoptosis by increasing ratio of Bcl-2/Bax and inhibiting caspase signaling pathway in SH-SY5Y cells. SSM demonstrated a neuroprotective effect on the simulated cerebral ischemia in vitro model, and this effect was the inhibition of mitochondria-mediated apoptosis pathway by scavenging of ROS generation. Therefore, SSM may be a promising neuroprotective strategy against ischemic stroke.

• 대한영상의학회지
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• 제81권6호
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• pp.1478-1485
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• 2020

리 증후군 또는 아급성 괴사성 뇌병증은 드물며, 빠르게 진행하는 신경 퇴행성 장애이다. 일반적으로 생후 1년 이내 호흡곤란, 심장기능 저하 등과 같은 증상이 발생하여, 2~3년 동안 환자의 75%가 사망에 이르는 심각한 질환이다. 리 증후군의 원인은 DNA mutation으로, 약 75%의 환자에서 핵 데옥시리보핵산의 돌연변이가 나타나고, 25%의 환자에서 미토콘드리아 데옥시리보핵산의 돌연변이가 발견된다. 임상 증상은 영향을 받은 뇌 영역에 따라 달라지며, 신경영상은 리 증후군 환자의 진단에 있어 중요한 역할을 한다. 성인에서 발생한 리 증후군은 더욱 드물고 어린 나이에 발생한 경우보다 더 느리게 진행한다. 우리는 성인에서 발생한 베르니케 뇌병증으로 오인된 리 증후군 환자의 증례를 보고하고자 한다.