• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.3
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• pp.347-355
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• 2015

Oxidative stress is one of the key mechanisms involved in neuronal damage. Neuroprotective effects and underlying mechanisms of action of several wild vegetables, Cirsium setidens (CS), Pleurospermum kamtschaticumin (PK), and Allium victorials (AV), against oxidative stress induced by hydrogen peroxide in SK-N-SH cells were investigated. CS and AV up to $400{\mu}g/mL$ showed no detectable effects on cell viability of human SK-N-SH neuro-blastoma cells compared with control. Incubation of SK-N-SH cells with hydrogen peroxide resulted in significant induction of cell death and reaction oxygen species (ROS) production, whereas treatment of cells with CS and AV significantly reduced cell death and ROS production, respectively. Among the wild vegetables tested, CS and PK showed more effective DPPH radical scavenging activity than AV, whereas PK showed strong cytotoxicity in SK-N-SH cells compared with the control. CS showed much higher inhibitory effects on cell death and ROS generation against oxidative stress than AV. Thus, CS was selected for subsequent experiments. Ethyl acetate (EA), hexane, butanol, aqueous, and chloroform extracts from CS significantly inhibited cell death and ROS generation in SK-N-SH cells induced by oxidative stress. EA extract from CS (CS-EA) showed the highest DPPH radical-scavenging activity, intra-cellular ROS-scavenging activity, and neuroprotective effects. CS-EA attenuated apoptosis signal-regulating p38 activation by inhibiting phosphorylation. The findings suggest that CS-EA protects neuronal cells through antioxidant activity and inhibition of phosphorylation of p38 in brain neural cells.

• Korean Journal of Biological Psychiatry
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• v.2 no.2
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• pp.252-256
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• 1995

Corticotropin-releasing factor(CRF)를 분비하는 배양세포주는 CRF의 세포내 조절을 연구하는데 있어 훌륭한 체계가 된다. BE(2)-M17 및 BE(2)-C 세포주는 CRF를 생산하고 분비하며 forskolin 처치에 반응하는 것으로 알려져 있다. 저자들은 이들 세포주에 phorbol 에스테르, 즉 phorbol 12-myristate 13-acetate(TPA) 0.8, 4, 10, 20 nM, 및 nitric oxide(NO)의 신호전달 경로의 자극제(1-${\mu}M$ nitroprusside)와 차단제($1{\mu}M$ nitroprusside+$300{\mu}M$ $N^G$-methyl-D-arginine), 그리고 interleukin-$1{\alpha}$ (IL $1{\alpha}$ ; 4, 20, 100, 500 pM)를 처치하여 CRF를 의미있게 증가시켰으나 세포외 분비는 C 세포에서만 변화되었다. NOS계의 자극제와 차단제는 C 세포의 forskolin 효과를 의미있게 변화시켰다. IL$1{\alpha}$는 두 세포주에 대한 영향이 없었다. 상기 제제들에 대한 이들 세포의 반응이 중추신경계 CRF 신경들과 관련하여 논의되었다.

• Journal of Oriental Neuropsychiatry
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• v.23 no.1
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• pp.129-143
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• 2012

Objectives : To evaluate the neuroprotective effects of the essential oil from Sohaphwangwon (SH), a Chinese traditional medicinal prescription in a Parkinson's disease mouse model. Methods : 1. The neuroprotective effect of SH on primary neuronal cells was examined by using 1-methyl-4-phenylpyridinium ion (MPP+). 2. The neuroprotective effect of SH 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. SH inhalation was applied before MPTP treatment for 7 days and continued until 12 days after the first MPTP treatment. 3. To find out the intracellular target signal molecule(s) regarding the neuroprotective effect of SH essential oil, brain-derived neurotropic factor (BDNF) and synaptic protein SNAP25 were examined by Western blot analysis. Results : 1. MPP+ induced a concentration-dependent decrease in cell viability. However, in the presence of 3 and 5 ug/ml of SH, MPP+-induced cell death was significantly reduced. 2. SH inhalation in MPTP mice led to the restoration of behavioral impairment and rescued tyrosine hydroxylase (TH)-positive dopaminergic neurodegeneration. 3. In SH / MPTP mice, BDNF and SNAP25 increased. Conclusions : This experiment suggests that the neuroprotective effect of SH essential oil is mediated by the expression of BDNF. Furthermore, SH essential oil may serve as a potential preventive or therapeutic agent regarding Parkinson's disease.

• Journal of Genetic Medicine
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• v.6 no.1
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• pp.25-37
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• 2009

Hereditary peripheral neuropathies can be categorized as hereditary motor and sensory neuropathies (HMSN), hereditary motor neuropathies (HMN), and hereditary sensory neuropathies (HSN). HMSN, HMN, and HSN are further subdivided into several subtypes. Here, we review the most recent findings in the molecular diagnosis and therapeutic strategy for hereditary peripheral neuropathies. The products of genes associated with hereditary peripheral neuropathy phenotypes are important for neuronal structure maintenance, axonal transport, nerve signal transduction, and functions related to the cellular integrity. Identifying the molecular basis of hereditary peripheral neuropathy and studying the relevant genes and their functions is important to understand the pathophysiological mechanisms of these neurodegenerative disorders, as well as the processes involved in the normal development and function of the peripheral nervous system. These advances and the better understanding of the pathogenesis of peripheral neuropathies represent a challenge for the diagnoses and managements of hereditary peripheral neuropathy patients in developing future supportive and curative therapies.

• Proceedings of the Korean Society of Medical Physics Conference
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• 2002.09a
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• pp.345-351
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• 2002

The purpose of this study was to assess clinical proton MR spectroscopy (MRS) as a noninvasive method for evaluating brain tumor malignancy at 3T high field system. Using 3T MRI/MRS system, localized water-suppressed single-voxe1 technique in patients with brain tumors was employed to evaluate spectra with peaks of N-acetyl aspartate (NAA), choline-containing compounds (Cho), creatine/phosphocreatine (Cr) and lactate. On the basis of Cr, these peak areas were quantificated as a relative ratio. The variation of metabolites measurements of the designated region in 10 normal volunteers was less than 10%. Normal ranges of NAA/Cr and Cho/Cr ratios were 1.67${\pm}$018 and 1.16${\pm}$0.15, respectively. NAA/Cr ratio of all tumor tissues was significantly lower than that of the normal tissues (p=0.005), but Cho/Cr ratio of all tumor tissue was significantly higher (p=0.001). Cho/Cr ratio of high-grade gliomas was significantly higher than that of low-grade gliomas (P=0.001). Except 4 menigiomas, lactate signal was observed in all tumor cases. The present study demonstrated that the neuronal degradation or loss was observed in all tumor tissues. Higher grade of brain tumors was correlated with higher Cho/Cr ratio, indicating a significant dependence of Cho levels on malignancy of gliomas. Our results suggest that clinical proton MR spectroscopy could be useful to predict tumor malignancy.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.1
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• pp.9-21
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• 2015

Cancer, a serious public health problem in worldwide, results from an excessive and uncontrolled proliferation of the body cells without obvious physiological demands of organs. The gastrointestinal tract, including the esophagus, stomach and intestine, is a unique organ system. It has the highest cancer incidence and cancer-related mortality in the body and is influenceed by both genetic and environmental factors. Among the various chemical elements recognized in the nature, some of them including zinc, iron, cobalt, and copper have essential roles in the various biochemical and physiological processes, but only at low levels and others such as cadmium, lead, mercury, arsenic, and nickel are considered as threats for human health especially with chronic exposure at high levels. Cadmium, an environment contaminant, cannot be destroyed in nature. Through impairment of vitamin D metabolism in the kidney it causes nephrotoxicity and subsequently bone metabolism impairment and fragility. The major mechanisms involved in cadmium carcinogenesis could be related to the suppression of gene expression, inhibition of DNA damage repair, inhibition of apoptosis, and induction of oxidative stress. In addition, cadmium may act through aberrant DNA methylation. Cadmium affects multiple cellular processes, including signal transduction pathways, cell proliferation, differentiation, and apoptosis. Down-regulation of methyltransferases enzymes and reduction of DNA methylation have been stated as epigenetic effects of cadmium. Furthermore, increasing intracellular free calcium ion levels induces neuronal apoptosis in addition to other deleterious influence on the stability of the genome.

• Korean Journal of Biological Psychiatry
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• v.5 no.2
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• pp.227-234
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• 1998

Objective : Many evidences suggest that patients with bipolar disorder have functional abnormalities in their postreceptor signal transduction pathways, and mood stabilizing effect of lithium is exerted by modulating this dysfunctioning system. Carbamazepine, an antiepileptic agent, is also known to be effective in the treatment and prevention of bipolar disorder. But the precise mechanism of action of the drug is still poorly understood. This study was performed to elucidate the possible therapeutic mechanism of carbamazepine. Method : The effects of chronic carbamazepine administration on protein kinase A and protein kinase C activities in frontal cortex of rat brain after 2 weeks of drug administration were measured and compared with those of control subjects. Results : Mean(${\pm}SE$) value of activity(phosphate transfer ${\mu}mol/mg$ of $protein{\cdot}min$) of protein kinase A in control and test group was $0.249563{\pm}0.036$ and $0.539853{\pm}0.078$, and that of protein kinase C was $0.654817{\pm}0.053$ and $1.146205{\pm}0.052$ respectively, being increased in test group. And differences between the two groups were statistically significant for both enzymes(protein kinase A ; p<0.01, protein kinase C ; p<0.001). Conclusion : These results show that chronic carbamazepine administration increases protein kinase A and C activities, and concerning the possible mode of therapeutic action in bipolar disorder it is suggested that enhanced enzymes phosphorylate receptor-G-protein-effector complexes to dampen hyperfunctioning neuronal activity and thus stabilize the system.

• Toxicological Research
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• v.22 no.4
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• pp.411-416
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• 2006

This study was carried out to investigate the spaciotemporal plasticity of intergeniculate leaflet in postnatal mongolian gerbil using genetically modified pseudorabies virus recombinant, which was a kind of excellent neurotracer with the ability to transpass the neuronal synaptic cleft. In addition, we tried to evaluate the special role of intergeniculate leaflet as a signal controler of circardian rhythm by expression of various nourotransmitters in suprachiasrnatic nucleus. The PRV-BaBlu, a genetically modified strain of PRV-Bartha with lac-Z gene, was injected into vitreous body of postnatal mongolian gerbil, and immunostained. The PRV-Bablu infected the neurons in intergeniculate leaflet of postnatal mongolian gerbil, and the degree of viral infection in postnatal period of experimental animals had tendency to increase with time consuming. This results showed that the mutant PRV-Bar-tha strain with lac-Z gene, PRV-BaBlu, was a very excellent neurotracer to localize the retinogeniculate tract with infection of neurons in intergeniculate leaflet specially.

• Journal of Applied Biological Chemistry
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• v.63 no.2
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• pp.137-145
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• 2020

Oxidative stress is one of the pathogenic mechanisms of various neurodegenerative diseases, such as Alzheimer's disease. Neuroglia, the most abundant cells in the brain, is thought to play an important role in the antioxidant defense system and neuronal metabolic support against neurotoxicity and oxidative stress. We investigated the protective effect of paeoniflorin (PF) against oxidative stress in C6 glial cells. Exposure of C6 glial cells to hydrogen peroxide (H₂O₂, 500 μM) significantly decreased cell viability and increased amounts of lactate dehydrogenase (LDH) release, indicating H₂O₂-induced cellular damage. However, treatment with PF significantly attenuated H₂O₂-induced cell death as shown by increased cell survival and decreased LDH release. The H₂O₂-stimulated reactive oxygen species production was also suppressed, and it may be associated with improvement of superoxide dismutase activity by treatment with PF. In addition, an increase in ratio of Bcl-2/Bax protein expression was observed after treatment with PF. In particular, the down-stream of the apoptotic signaling pathway was inhibited in the presence of PF, mostly by reduction of cleaved-poly ADP ribose polymerase, cleaved caspase-3, and -9 protein expression. Furthermore, H₂O₂-induced phosphorylation of c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 was attenuated by treatment with PF. Taken together, neuroprotective effect of PF against oxidative stress probably result from the regulation of apoptotic pathway in C6 glial cells. In conclusion, our findings suggest that PF may be a potent therapeutic agent for neurodegenerative disorders.

• The Korean Journal of Zoology
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• v.38 no.4
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• pp.542-549
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• 1995

The effect of extraceflular matrix (ECM) protein on the neuronai differentiation of SI(-N-SH and IMR-32 human neuroblastoma cell lines was examined. When ceils were cultured on the laminin/collagen coated plate for 7 days, the extensive neurite outgrowth was observed In IMR-32. To address the reason why IMR-32 cell llne did not respond to ECM proteins, the ECM mediated early signalling mechanisms were analysed in both SK-N-SH and IMR-32. When cells were plated on the laminin/collagen coated plates, tyrosine phosphorylated proteins were Increased within an hour In both of these cells. Moreover, the foaal adhesion IlInase (FAK) was tyrosine phosphorylated in both of these two cell lines. These results suggest that the ECM mediated early signalling mechanism was normal in IMR-32 cell line. The expression of both NSE and Bcl-2 was increased by ECM treatment in SK-N-SH. However, these components were not changed by ECM In IMR 32 cells to ECM component Is likely due to the abnomality of the transcriptional regulation mechanism which Is responsible for the neuronal differentiation.