• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1810-1820
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• 2004

The purpose of this study was to estimate the effects of Ramulus et Uncus Uncariae DM fraction on CT105-injuried neuronal cells. We were examined by ROS formation, neurite outgrowth assay and DPPH scravage assay. Additionally, we investigated the association between the CT105 and neurite degeneration caused by CT105-induced apoptotic response in neurone cells. We studied on the regeneratory and inhibitory effects of anti-Alzheimer disease in pCT105-induced neuroblastoma cell lines by REUD. Findings from our experiments have shown that REUD inhibits the synthesis or activities of CT105, which has neurotoxityies and apoptotic activities in cell line. In addition, treatment of REUD(>50㎍/㎖ for 12 hours) partially prevented CT105-induced cytotoxicity in SK-N-SH cell lines, and were inhibited by the treatment with its. REUD(>50㎍/㎖ for 12 hours) repaired CT105-induced neurite outgrowth when SK-N-SH cell lines was transfected with CT105. As the result of this study, In REUD group, the apoptosis in the nervous system was inhibited, the repai: against the degeneration of Neuroblastoma cells by CT105 expression was promoted. Base on these findings, REUD may be beneficial for the treatment of AD.

• The Journal of Korean Medicine
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• v.26 no.3 s.63
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• pp.135-145
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• 2005

Objectives : This study investigated effect of Evodiae fructus water extract (EVOR) on apoptotic cell death induced by NaCN in SK-N-SH neuroblastoma cell lines. NaCN stimulates glutamate release which can activate glutamate receptors to initiate excitotoxic processes. This study examines the role of EVOR in mediating NaCN-induced cytotoxicity. Methods & Results : Cytotoxicity was assessed by measuring lactate dehydrogenase (LDH) in the culture media. NaCN(0.1mM) produced cytotoxicity following 12hrs of incubation. NaCN-induced cytotoxicity was partially blocked by EVOR. The treatment of EVOR in simultaneous exposure of cultures to NaCN provided complete protection against cytotoxicity. NaCN-induced cytotoxicity was found to inhibit DNA fragmentation, repaired by cell cycle and simultaneous exposure to NaCN, regenerated with neurite outgrowh by EVOR. These results indicate thaf damage by NaCN in neumnal cell cultures was repaired by EVOR, whereas NaCN-induced cytotoxicity is blocked Primarily by activation of anti-apoptosis. Conclusions : These results suggest that EVOR may be beneficial for the treatment of dementia and other degenerative problems of the central nervous system.

• Korean Journal of Food Science and Technology
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• v.36 no.6
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• pp.974-978
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• 2004

Brown-alga-derived natural agent NX42, mainly composed of algal polysaccharides and phlorotannins, showed mild but dose-dependent inhibition of acetylcholinesterase with $IC_{50}=600-700\;{\mu}g/mL$. Phlorotannin-rich fraction of NX42 showed substantial increase of the activity by more than one order of magnitude ($IC_{50}=54\;{\mu}g/mL$) and significant protection of SK-N-SH cells from oxidative stress by $H_2O_2$. Learning trials of mice for 5 consecutive days revealed electric-shock treatment during learning period significantly retarded learning process, whereas NX42-treated mice showed significant resistance against leaning deficiency possibly mainly due to anticholinesterase and neuroprotective activities of phlorotannin.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.4
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• pp.1037-1049
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• 2003

Numerous lines of evidence indicate that some of the neurotoxicity associated with Alzheimer's disease (AD) is due to proteolytic fragments of the amyloid precursor protein (APP). Most research has focused on the amyloid 6 (M). However, the possible role of other cleaved products of APP is less clear. Lately It has been reported that a recombinant carboxy-terminal 105 amino acid fragment (CT105) of APP induced strong nonselective inward currents in Xenopus oocyte. In a brain with Alzheimer's disease (AD), to investigate the roles of carboxyl-terminal fragment (CT105) of amyloid precursor protein (APP) in apoptosis processes possibly linked to neurodegeneration associated with AD, we examined the effects of the CT of APP with 105 amino acid residues (CT105) on the alteration of apoptosis triggers in neubroblastoma cells. We have investigated whether Radix Polygalae and Rhizoma Acori Graminei mixture extract (RP+RAG) inhibits CT105-induced apoptosis of neuroblastoma cells. We found that RP+RAG inhibits CT105-induced apoptosis in SK-N-SH cells. Treatment of the cells with RP+RAG inhibited CT105-induced DNA fragmentation and Tunel assay of nuclear chromatin and inhibited the caspase-3 expression in SK-N-SH cells. As the result of this study, In RP+RAG group, the apoptosis in the nervous system is inhibited, the repair against the degerneration of neuroblastoma cells by CT105 expression is promoted. These results indicate that RP+RAG possess strong inhibitory effect of apoptosis in the nervous system and repair effect against the degeneration of neuroblastoma cells by CT105 expression

• Biomolecules & Therapeutics
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• v.11 no.4
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• pp.214-223
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• 2003

Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA) have become popular recreational drugs of abuse in many countries. Although the neurotoxic damage caused by METH and MDMA is characterized by degeneration of the dopaminergic and serotonergic systems in brain, the molecular and cellular mechanisms remain to be clarified. Therefore, the purposes of this study were to confirm the capability of METH and MDMA to induce apoptosis and to clarify the action of its molecular mechanism by using serotonergic JAR cells and dopaminergic SK-N-SH cells. METH and MDMA were dose-dependently cytotoxic to human serotonergic JAR cells and dopaminergic SK-N-SH cells. The morphological change of apoptosis was found in Giemsa staining and TUNEL and further verified in DNA fragmentation analysis. Immunoblotting analysis revealed proteolytic cleavage of caspase-3 and -9 and change of bcl-2 and bax proteins. These results suggest that METH and MDMA may induce caspase-dependent apoptosis via the mitochondrial cell death pathway and METH and MDMA-induced neurotoxicity may happen to broadly and independently of both dopaminergic and serotonergic systems.

• Journal of Ginseng Research
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• v.39 no.1
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• pp.69-75
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• 2015

Background: Ginseng has been shown to exert antistress effects both in vitro and in vivo. However, the effects of ginseng on stress in brain cells are not well understood. This study investigated how Korean Red Ginseng (KRG) controls hydrogen peroxide-induced apoptosis via regulation of phosphatidylinositol-3 kinase (PI3K)/Akt and estrogen receptor (ER)-${\beta}$ signaling. Methods: Human neuroblastoma SK-N-SH cells were pretreated with KRG and subsequently exposed to $H_2O_2$. The ability of KRG to inhibit oxidative stress-induced apoptosis was assessed in MTT cytotoxicity assays. Apoptotic protein expression was examined byWestern blot analysis. The roles of ER-${\beta}$, PI3K, and p-Akt signaling in KRG regulation of apoptosis were studied using small interfering RNAs and/or target antagonists. Results: Pretreating SK-N-SH cells with KRG decreased expression of the proapoptotic proteins p-p53 and caspase-3, but increased expression of the antiapoptotic protein BCL2. KRG pretreatment was also associated with increased ER-${\beta}$, PI3K, and p-Akt expression. Conversely, ER-${\beta}$ inhibition with small interfering RNA or inhibitor treatment increased p-p53 and caspase-3 levels, but decreased BCL2, PI3K, and p-Akt expression. Moreover, inhibition of PI3K/Akt signaling diminished p-p53 and caspase-3 levels, but increased BCL2 expression. Conclusion: Collectively, the data indicate that KRG represses oxidative stress-induced apoptosis by enhancing PI3K/Akt signaling via upregulation of ER-${\beta}$ expression.

• Proceedings of the Zoological Society Korea Conference
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• 1996.10a
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• pp.224.2-224
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• 1996

No Abstract, See Full Text

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.124.1-124.1
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• 2003

We investigated whether the mushroom extracts can protect neuronal death and ameliorate memory deficits in Alzheimer"s disease induced by $\beta$-amyloid peptide[A$\beta$(25-35)]. Cellular model of Alzheimer"s disease was produced by using SK-N-SH human neuronal cells treated with $A\beta$. Treatment with 40uM $A\beta$ for 48hours caused a 46% loss of cell viability. First, we examined the effects of 22 mushroom extracts on neuronal death using MTT assay. We found that 3 mushroom extracts increased viability of the cells from 46% to 87%. (omitted)

• The Journal of Korean Medicine
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• v.26 no.3 s.63
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• pp.27-42
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• 2005

Objectives : Alzheimer's disease (AD) is a progressive and fatal neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles. These plaques are associated with degenerating neuronal processes and consist primarily of fibrillary aggregates of beta-amyloid$ protein, generated from amyloid precursor protein (APP). Another amyloidogenic fragment, the carboxyl terminus (CT) of APP, which is composed of 99-105 amino acid residues containing the complete $A{\beta}$ sequence, also appears to be toxic to neurones. Recent evidence suggest that CT105, carboxy terminal 105 amino acids peptide fragment of APP, may be an important factor causing neurotoxicity in AD. Methods : Although a variety of oriental prescriptions including Pinelliae rhizoma have traditionally been utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet been fully elucidated. In the present study, we investigated effects of the dichloromethane extract of Pinelliae rhizoma (PINR) on neurotoxicity and the formation of reactive oxygen species (ROS) and nitric oxide (NO) in SK-N-SH cells overexpressed with CT105. In addition, we evaluated its radical scavenging activity and effects on acetylcholinesterase (AChE) activity. Furthermore, effects on cognitive deficits induced by scopolamine treatment in rats were evaluated. Results ; We found in this study that PINR significantly inhibited apoptotic neuronal death induced by CT105 overexpression in SK-N-SH cells. Based on morphological examinations by phase-contrast microscopy, PINR reversed apoptotic changes of CT105-expressed cells. It was also found that PINR significantly promoted neurite outgrowth and inhibited formation of ROS nd NO. PINR was shown to scavenge DPPH radicals and noncompetitively inhibit AChE activity. Furthermore, it reduced scopolamine-induced memory impairment in rata, assessed by passive avoidance test. Conclusions : Taken together, these results demonstrate that PINR exhibits neuroprotective, antioxidant, and memory enhancing effects, and therefore may bs beneficial for the treatment of AD.

• Journal of Life Science
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• v.23 no.1
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• pp.84-94
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• 2013

The cytotoxicity of coffee-like green tea (CLGT) was determined in a human breast cancer cell line, MCF-7; a human prostate cancer cell clone, PC-3; a human neuroblastoma cell line, SK-N-SH; and a rat cardiomyoblast cell line, H9c2, with reference to green tea leaves (GTL). The CLGT was prepared by roasting the GTL for 60 min at $240^{\circ}C$ in a temperature-controlled frying pan. The CLGT preparation imitated the flavor and taste characteristics of coffee fairly well according to sensory analysis. The CLGT preparation had no adverse cytotoxic effects on the cancer cells or the normal cells compared to GTL. No significant change in the antioxidant activity was seen in the CLGT preparation compared to that of GTL. The amount of total protein, sugar, and phenolic compounds was reduced in the preparation relative to those in GTL, a fact that might explain the coffee-like flavor and/or taste characteristics of the CLGT preparation. These results suggest that CLGT prepared by roasting GTL for 60 min at $240^{\circ}C$ does not show any adverse effects on cancer cells and normal cells compared to GTL. They imply that CLGT could be safe for human consumption.