• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.11a
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• pp.153-153
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• 2002

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.53.1-53.1
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• 2008

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.153-153
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• 2002

Methylmercury (MeHg), one of the heavy metal compound, can cause severe damage to the central nervous system in humans. Many reports have contributed MeHg poisoning to contaminated foods and release into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established.(omitted)

• Archives of Pharmacal Research
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• v.16 no.2
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• pp.155-157
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• 1993

DNA transfection conditions were investigated by calcium phosphate-DNA co-precipitation in SK-N-BE(2)C human neuroblastoma cells. The DNA plasmid of TH2400CAT was used in which rat tyrosine hydroxylase gene was inserted into chloramphenicol acetyltransferase reporter gent. The transfection efficiency was 25-30% and the method was simple and reproducible. So, the method will be a good tool for transient transfection analysis.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.196.2-197
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• 2003

Parkinson's disease (PO) is a widespread neurodegenerative disorder. Even though PD has been studied in many aspects, it is still unknown the molecular signaling mechanisms linking reactive oxygen species (ROS) and neuronal apoptosis in PD. A better understanding of cellular mechanisms that occur in Parkinson's disease is essential for development of new therapies. In this study we investigated the signaling molecules involved in neuronal apoptosis induced by 6-hydroxydopamine (6-OHDA) in human SK-N-SH neuroblastoma cells as a model cellular system. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.123.2-123.2
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• 2003

The cellular mechanisms by which excess exposure to the excitatory neurotransmitter glutamate can produce neuronal injury are unknown. In this study, we found that glutamate induced cell death at IC (50) of 100 microM on the cultured human SH-SY5Y neuroblastoma cells. It has been hypothesized that glutamate excitotoxicity is related with the elevation of calcium (Ca) levels. To determine the dependence of glutamate neurotoxicity on Ca environment, extracellular (EDTA) and intracellular (BAPTA/AM) chelator were used. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.139.1-139.1
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• 2003

Since radiotherapy has been suspected to promote tumor metastasis and the presence of increase levels of adhesion molecules have implications for metastasis, we decided to investigate whether gamma-irradiation alters the expression of intercellular adhesion molecule-1 (ICAM-1) on neuroblastoma cells and the activities of relevant intracellular signaling molecules. In the present study, the relative of ICAM-1 expression under gamma-irradiated neuroblastoma cells were assessed by Western blot analysis. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.691-697
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• 1997

The mechanisms underlying opiate tolerance and dependence are not fully understood. We used human neuroblastoma SH-SY5Y cells as a model system for studying effects of morphine tolerance and withdrawal on c-myc induction and cAMP levels. It has been reported that regulation of c-fos by acute and chronic morphine withdrawal is mediated through alterations in CREB transcription factor. In this study, we examined the effects of morphine tolerance on c-myc expression and cAMP concentrations. The activation of opiate receptors by an acute morphine administration resulted in an increase in c-myc mRNA and a decrease in cAMP concentrations in a dose-dependent manner $(5,\;10,\;15,\;and\;20\;{\mu}M)$. On the other hand, the chronic treatment of morphine $(10\;{\mu}M\;for\;six\;days)$ did not induce the elevated expression of c-myc mRNA. The c-myc expression was slightly inhibited in comparison with that of the acute morphine response. However, cAMP concentrations were increased with regard to morphine withdrawal response. These results suggest that the alterations in c-myc expression might imply a significant opiate regulation relating to morphine tolerance. This observation differs from increased expression of c-fos via regulation of cAMP pathway.

• International Journal of Oral Biology
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• v.35 no.2
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• pp.69-74
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• 2010

The mu opioid receptor (MOR) has been regarded as the main site of interaction with analgesics in major clinical use, particularly morphine. The repressor element-1 silencing transcription factor (REST) functions as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it is expressed in certain mature neurons, suggesting that it may have complex and novel roles. In addition, the interactions between MOR and REST and their functions remain unclear. In this study, we examined the effects of morphine on the expression of REST mRNA and protein in human neuroblastoma NMB cells to investigate the roles of REST induced by MOR activation in neuronal cells. To determine the effects of morphine on REST expression, we performed RT-PCR, real-time quantitative RT-PCR, western blot analysis and radioligand binding assays in NMB cells. By RTPCR and real-time quantitative RT-PCR, the expression of REST was found to be unchanged by either the MOR agonist morphine or the MOR specific antagonist CTOP. By western blot, morphine was shown to significantly inhibit the expression of REST, but this suppression was completely blocked by treatment with CTOP. In the radioligand binding assay, the overexpression of REST led to an increased opioid ligand binding activity of endogenous MOR in the NMB cells. These results together suggest that morphine inhibits the expression of REST in human neuroblastoma cells through a post-transcriptional regulatory mechanism mediated through MOR.

• Molecules and Cells
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• v.38 no.7
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• pp.630-637
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• 2015

Morus alba root extract (MARE) has been used to treat hyperglycaemic conditions in oriental medicine. Here, we studied whether MARE possesses a cytotoxic effect on neuroblastoma. To check the cytotoxicity generated by MARE was whether relatively higher against the cancer cells rather than normal cells, we chose a neuroblastoma cell line (B103) and a normal cell line (Rat-2). A CCK assay revealed that MARE ($10{\mu}g/ml$) reduced cell viability to approximately 60% compared to an untreated control in B103 cells. But in Rat-2 cells, MARE induced relatively lower cytotoxicity. To investigate the mechanisms underlying the cytotoxic effect of MARE, we used flow cytometry combined with immunoblot analyses. We found that MARE-treatment could accumulate ROS and depolarize mitochondria membrane potential of B103 cells. Further treatment with MARE in B103 cells also could damage DNA and induce apoptosis. An expression study of p-Akt also suggested that there was a reduction in cellular proliferation and transcription along with the process of apoptosis, which was further evidenced by an increase in Bax and cleaved-caspase 3 activity. Together, our findings suggest that MARE produces more cytotoxicity in cancer cells while having a relatively attenuated effect on normal cells. As such, MARE may be a safer option in cancer therapeutics, and it also shows potential for the patients with symptoms of hyperglycemia and cancer.