• 제목/요약/키워드: Neuronal death

검색결과 521건 처리시간 0.023초

미토콘드리아 기능을 통해 내인성 글루탐산이 신경세포 생존에 미치는 영향 (Endogenous glutamate enhances survival rates of neurons via activating mitochondrial signalings in hippocampal neuron)

  • 노진우;김혜지;은수용;강문석;정성철;양윤실
    • 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.

Glutamate 매개 흥분성 신경독성에 대한 봉독의 NSC-34 신경세포사멸 억제 효과 (Effect of Bee Venom on Glutamate-mediated Excitotoxicity in NSC-34 Motor Neuronal Cells)

  • 이상민;최선미;정소영;양은진
    • 약학회지
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    • 제55권5호
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    • pp.385-390
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    • 2011
  • Bee venom (BV), which is extracted from honeybees, has been used in traditional Korean medical therapy. Glutamate-mediated excitotoxicity contributes to neuronal death in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) or Alzheimer's disease (AD). This study is to investigate the effect of BV on glutamate-induced neurotoxicity on NSC-34 motor neuron cells. To determine the viability of motor neuronal cells, we performed with MTT assays in glutamate-treated NSC-34 cell with BV or without. For the measurement of oxidative stress, DCF assay was used in glutamate-treated NSC-34 motor neuronal cells with BV or without. To investigate the molecular mechanism of BV against glutamate-mediated neurotoxicity in NSC-34 cells, western blot analysis was used. Glutamate significantly decreased cell viability by glutamate dose- or treatment time-dependent manner in NSC-34 cells. However, BV pre-treatment dramatically inhibited glutamate-induced neuronal cell death. Furthermore, we found that BV increased the expression of Bcl-2 protein that is anti-apoptotic protein and reduced the generation of oxidative stress. BV has a neuroprotective role against glutamate neurotoxicity by an increase of anti-apoptotic protein. It suggests that BV may be useful for the reduction of neuronal cell death in neuronal disease models.

Ginsentology I: Differential Ca2+ Signaling Regulations by Ginsenosides in Neuronal and Non-neuronal cells

  • Lee, Jun-Ho;Nah, Seung-Yeol
    • Journal of Ginseng Research
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    • 제30권2호
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    • pp.57-63
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    • 2006
  • One of the various signaling agents in the animal cells is the simple ion called calcium, $Ca^{2+}$.$Ca^{2+}$ controls almost everything that animals do, including fertilization, secretion, metabolism, muscle contractions, heartbeat, learning, memory stores, and more. To do all of this, $Ca^{2+}$ acts as an intracellular messenger, relaying information within cells to regulate their activity. In contrast, the maintenance of intracellular high $Ca^{2+}$ concentrations caused by various excitatory agents or toxins can lead to the disintegration of cells (necrosis) through the activity of $Ca^{2+}$-sensitive protein-digesting enzymes. High concentrations of calcium have also been implicated in the more orderly programs of cell death known as apoptosis. Because this simple ion, acts as an agent for cell birth, life and death, to coordinate all of these functions, $Ca^{2+}$ signalings should be regulated precisely and tightly. Recent reports have shown that ginsenosides regulate directly and indirectly intracellular $Ca^{2+}$ level with differential manners between neuronal and non-neuronal cells. This brief review will attempt to survey how ginsenosides differentially regulate intracellular $Ca^{2+}$ signaling mediated by various ion channels and receptor activations in neuronal and non-neuronal cells.

SF508 Protects Ceramide-induced Neuronal Cell Death

  • Do Yeon Lee;Kwang Gill Lee;Joo-Hong Yeo;Hae Yong Kweon;Hee-Sun Chae;Yong Koo Kang;Wan Seok Joo;In Sook Lee;Sang Hyung Lee
    • 한국잠사학회:학술대회논문집
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    • 한국잠사학회 2003년도 International Symposium of Silkworm/Insect Biotechnology and Annual Meeting of Korea Society of Sericultural Science
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    • pp.109-111
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    • 2003
  • In the present study, we examined ceramide-induced neuronal cell death and its mechanism and process using SK-N-KH cells, and investigated whether ROS was produced and related to other factors. In addition, we tried to check whether silk fibroin had protective effect fur neuronal cells, and through which cell death process this protective mechanism functioned. (omitted)

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Brief comparison of the mechanism of modern medicine and traditional medicine in neuronal cell death

  • Kim, Young-Sick;Jeong, Hyun-Ja;Kim, Hyung-Min;Cho, Seung-Hun
    • 셀메드
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    • 제1권1호
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    • pp.1.1-1.7
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    • 2011
  • Medicine has a past, a present, and will have a future; the same can be said for many diseases. Even with the surprising development of modern medicine, traditional medicine, especially eastern Asian traditional medicines still exist and are widely used in those regions. But modern medicine and western pacific traditional medicines have different theories and applications for the same disease. In this review, traditional medical theory, used together with modern medicine, can be combined to shed light on the area of neuronal death.

Neuroprotective Effect of Ginseng radix on ICH-induced Rats

  • Jang, Kwan-Ho;Song, Yun-Kyung;Lim, Hyung-Ho
    • 대한한의학회지
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    • 제26권4호
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    • pp.87-97
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    • 2005
  • Backgrounds: Intracerebral hemon-hage is one of the most devastating types of stroke. Ginseng radix, the root of Panax Ginseng, C. A. MEYER (Araliaceae), is one of the most famous medicinal herbs with various therapeutic applications. Objectives: In the present study, the effect of aqueous extract of Ginseng radix on intracerebral hemorrhage-induced neuronal cell death in rats was investigated. Materials and Methods: Step-down avoidance task, Nissl staining, immunohistochemistry for caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were used for this study. Results: The present results show that hemorrhage-induced lesion volume and apoptotic neuronal cell death in the striatum were significantly suppressed by treatment with Ginseng radix, resulting in enhancement of short-ten-n memory. Conclusions: We have shown that Ginseng radix has a neuroprotective effect on stroke, and aids the recovery from central nervous system sequelae following stroke.

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Epicatechin Prevents Methamphetamine-Induced Neuronal Cell Death via Inhibition of ER Stress

  • Kang, Youra;Lee, Ji-Ha;Seo, Young Ho;Jang, Jung-Hee;Jeong, Chul-Ho;Lee, Sooyeun;Jeong, Gil-Saeng;Park, Byoungduck
    • Biomolecules & Therapeutics
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    • 제27권2호
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    • pp.145-151
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    • 2019
  • Methamphetamine (METH) acts strongly on the nervous system and damages neurons and is known to cause neurodegenerative diseases such as Alzheimer's and Parkinson's. Flavonoids, polyphenolic compounds present in green tea, red wine and several fruits exhibit antioxidant properties that protect neurons from oxidative damage and promote neuronal survival. Especially, epicatechin (EC) is a powerful flavonoid with antibacterial, antiviral, antitumor and antimutagenic effects as well as antioxidant effects. We therefore investigated whether EC could prevent METH-induced neurotoxicity using HT22 hippocampal neuronal cells. EC reduced METH-induced cell death of HT22 cells. In addition, we observed that EC abrogated the activation of ERK, p38 and inhibited the expression of CHOP and DR4. EC also reduced METH-induced ROS accumulation and MMP. These results suggest that EC may protect HT22 hippocampal neurons against METH-induced cell death by reducing ER stress and mitochondrial damage.

Increase of Cdk5 and p35 during Retinoic Acid-Induced Neuronal Differentiation of SK-N-BE(2)C cells

  • Lee, Jong-Hee;Kim, Kyung-Tai
    • 한국생물물리학회:학술대회논문집
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    • 한국생물물리학회 2002년도 제9회 학술 발표회 프로그램과 논문초록
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    • pp.46-46
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    • 2002
  • Cdk5, a neuronal Cdc2-like kinase, exhibits a variety of functions in neuronal differentiation and neurocytoskeleton dynamics as well as neuronal degeneration and cell death. However, its role in retinoic acid (RA)-induced differentiation has not been reported yet. We newly found that RA treatment of SK-N-BE(2)C, human neuroblastoma, increased expression of Cdk5 concomitantly with a neuronal specific activator, p35.(omitted)

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배양된 대뇌피질세포에서 산화성 손상에 대한 6R-Tetrahydrobiopterin의 억제작용 (Study on the Protective Effects of 6R-Tetrahydrobiopterin on the Oxidative Neuronal Injury in Mouse Cortical Cultures)

  • 문경섭;이제혁;강삼석;김수한;김재휴;정신;김태선;이정길
    • Journal of Korean Neurosurgical Society
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    • 제30권9호
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    • pp.1059-1064
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    • 2001
  • Objective : 6R-Tetrahydrobiopterin(BH4) is a cofactor for the aromatic amino acid hydroxylases which is essential for the biosynthesis of catecholamines and serotonin. It also acts as a cofactor for nitric oxide synthase, and stimulates the release of some neurotransmitters such as dopamine, serotonin, acetylcholine and glutamate. Recently, it has been reported that BH4 could induce cellular proliferation and enhance neuronal survival. This study was performed to investigate the antioxidative effect of BH4 on the various oxidative insults in mouse cerebral cortical cell cultures. Methods : Iron ion(FeCl2), zinc ion(ZnCl2), sodium nitroprusside(SNP) and buthionine sulfoximine(BSO, a glutathione depletor) were used as oxidants. Cell death was assessed by measurement of lactate dehydrogenase efflux to bathing media at the end of exposure. Result : All 4 oxidants induced neuronal cell death associated with cell body swelling, which was markedly inhibited by trolox($100{\mu}M$), a vitamin E analog. BH4($10-100{\mu}M$) markedly inhibited the neuronal cell death induced by all 4 oxidants($20{\mu}M\;Cu^{2+}$, $20{\mu}M\;Zn^{2+}$, $1{\mu}M$ SNP or 1mM BSO). However, BH4 failed to inhibit the neuronal cell death induced by 24hr exposure to $20{\mu}M$ NMDA. Conculsion : These results suggest that BH4 has antioxidative action independently of any actions of enzyme cofactor.

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Effects of Glutamate Receptor Antagonists and Protein Synthesis Inhibitor on Delayed Neuronal Death Induced by Transient Global Ischemia in Rat Brain

  • Ko, Jun-Seog;Bae, Choon-Sang;Kim, Jong-Keun
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권3호
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    • pp.279-286
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    • 1998
  • It has been well documented that transient forebrain global ischemia causes selective neuronal degeneration in hippocampal CA1 pyramidal neurons with a delay of a few days. The mechanism of this delayed hippocampal CA1 pyramidal neuronal death (DND) is still controversial. To delineate the mechanisms of the DND, the effects of treatment with MK-801, an NMDA receptor antagonist, kynurenic acid, a NMDA/non-NMDA receptor antagonist, and/or cycloheximide, a protein synthesis inhibitor, on the DND were investigated in male Wistar rats. To examine the participation of apoptotic neuronal death in the DND, TUNEL staining was performed in ischemic brain section. Global ischemia was induced by 4-vessel occlusion for 20 min. All animals in this study showed the DND 3 and 7 days after the ischemic insult. The DND that occured 3 days and 7 days after the ischemia were not affected by pretreatment with MK-801 (1 mg/kg), but markedly attenuated by the pretreatment with kynurenic acid (500 mg/kg). Treatment with cycloheximide (1 mg/kg) also markedly inhibited the DND. The magnitudes of attenuation by the two drugs were similar. The magnitude of attenuation by co-treatments with kynurenic acid and cycloheximide was not greater than that with any single treatment. TUNEL staining was negative in the sections obtained 1 or 2 days after the ischemic insults, but it was positive at hippocampal CA1 pyramidal cells in sections collected 3 days after the ischemia. These results suggested that the DND should be mediated by the activation of non-NMDA receptor, not by the activation of NMDA receptor and that the activation of AMPA receptor should induce the apoptotic process in the DND.

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