• The Journal of Korean Medicine
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• v.20 no.4
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• pp.3-10
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• 2000

In order to elucidate the toxic mechanism of neurotoxical damage and neuroprotective effect of Jangwon-hwan(Zhuangyuan-wan) water extract, this experiment was performed. Neurotoxic effects of xanthine oxidase/hypoxanthine(XO/HX) were examined by MTT and NR assay, neuroprotective effects of Jangwon-hwan(Zhuangyuan-wan) water extract were examined by neurofilament enzymeimmuno assay(EIA). XO/HX induced an increase in cell viability, and a decrease in the amount of neurofilament on cultured mouse cerebral cortical neurons in dose-dependent manner. In neuroprotective effect of herb medicine, Jangwon-hwan(Zhuangyuan-wan) water extract increased the amount of neurofilament on cultured mouse cerebral cortical neurons damaged by XO/HX. From the results, it is suggested that XO/HX showed toxic effect in cultured mouse cerebral cortical Neurons and Jangwon-hwan(Zhuangyuan-wan) water extract is very effective in the prevention of neurotoxicity induced by XO/HX.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.117-117
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• 2003

Bee Venom (BV) has been treated in inflammatory diseases such as rheumatoid arthritis (RA). Bee venom contains several biologically active non-peptide substances as well as two major known peptides; the hemolytic peptide melittin (50%) and the neurotoxic peptide apamin, and a number of minor peptides.(omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.93.1-93.1
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• 2003

Bee Venom (BV) has been treated in inflammatory diseases such as rheumatoid arthritis (RA). Bee venom contains several biologically active non-peptide substances as well as two major known peptides; the hemolytic peptide melittin (50%) and the neurotoxic peptide apamin, and a number of minor peptides. Previous our study showed that BV blocked LPS and SNP-induced production of NO and PG through inactivation of NF-kB which regulates expression of COX-2 and iNOS. (omitted)

• Journal of Digestive Cancer Research
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• v.11 no.1
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• pp.45-48
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• 2023

One of the most common side effects of chemotherapeutic agents is chemotherapy-induced peripheral neuropathy (CIPN). The occurrence of CIPN is increasing as the survival rate of patients with cancer improves and the cumulative dose or duration of neurotoxic drugs increases. Approximately 30-40% of patients receiving neurologically toxic drugs experience CIPN, which eventually increases the burden of medical expenses. However, preventive measures against CIPN have not yet been established. Clinical trials have tested various drugs for the management of neuropathic pain, but only duloxetine has shown any significant effect. Further studies should evaluate nonpharmaceutical treatments, such as exercise.

• YAKHAK HOEJI
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• v.51 no.4
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• pp.264-269
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• 2007

Alzheimer’s disease (AD) is characterized pathologically by the presence of intracellular neurofibrillary tangles and deposition of ${\beta}-amyloid $ (A ${\beta}$) peptides, which are generated by processing of amyloid precursor protein (APP). It is urgent to develop effective therapies for the treatment of AD, since our society rapidly accelerate aging. A${\beta}$ peptides have been believed to be neurotoxic and now are also considered to have effects on the mechanism of memory formation. In this study, effects of radicicol on the metabolism of APP were analyzed. Radicicol inhibited the secretion of A${\beta}$ from the Neuro2a cell line (APPswe cell) expressing APPswe. Beta-site APP cleaving enzyme (BACE) fluorescence resonance energy transfer (FRET) assay revealed that it inhibited BACE activity in a dose dependently manner. Immunoblotting study showed that it inhibited intracellular heat shock protein (HSP)90 and it increased the secretion of HSP90 from the APPswe cells. We suggest that radicicol inhibits APP metabolism and Ap generation by the means of HSP90 inhibitory mechanism and partially BACE inhibitory mechanism. This is the first report that radicicol inhibits the secretion of A${\beta}$ peptides from neuroblastoma cells.

• Proceeding of EDISON Challenge
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• 2015.03a
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• pp.14-23
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• 2015

Alzheimer's disease is one of the most common types of degenerative dementia. As a considerable cause of Alzheimer's disease, neurotoxic plaques composed of 39 to 42 residue-long amyloid beta($A{\beta}$) fibrils have been found in the patient's brain in large quantity. A previous study found that erythrosine B (ER), a red color food dye approved by FDA, inhibits the formation of amyloid beta fibril structures. Here, in an attempt to elucidate the inhibition mechanism, we performed molecular dynamics simulations to demonstrate the conformational change of $A{\beta}40$ induced by 2 ERs in atomistic detail. During the simulation, the ERs bound to the surfaces of both N-terminus and C-terminus regions of $A{\beta}40$ rapidly. The observed stacking of the ERs and the aromatic side chains near the N-terminus region suggests a possible inhibition mechanism in which disturbing the inter-chain stacking of PHEs destabilizes beta-sheet enriched in amyloid beta fibrils. The bound ERs block water molecules and thereby help stabilizing alpha helical structure at the main chain of C-terminus and interrupt the formation of the salt-bridge ASP23-LYS28 at the same time. Our findings can help better understanding of the current and upcoming treatment studies for Alzheimer's disease by suggesting inhibition mechanism of ER on the conformational transition of $A{\beta}40$ at the molecular level.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.1
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• pp.57-62
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• 2013

Alzheimer's disease (AD), one of the most common forms of dementia, is characterized pathologically by the presence of intracellular neurofibrillary tangles and deposition of ${\beta}$-amyloid ($A{\beta}$) peptides of 40-42 residues, which are generated by processing of amyloid precursor protein (APP). $A{\beta}$ has been believed to be neurotoxic and now is also considered to have a role on the mechanism of memory dysfunction. Here, we show that MeOH extract from stem bark of Platycarya strobilacea Sieb. et. Zucc. (PSM) affects on the processing of APP from the APPswe over-expressing Neuro2a cell line. We found that PSM may regulate the processing of APP and increase the sAPP${\alpha}$. PSM does not change the protein level of presenilin and nicastrin, however, it reduces the protein expression level of BACE1. In addition, PSM reduces the secretion level of $A{\beta}42$ and $A{\beta}40$ from the cell line without toxicity. We suggest that Platycarya strobilacea may be useful as a herbal medicine to treat Alzheimer's disease.

• Korean Journal of Biological Psychiatry
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• v.15 no.3
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• pp.175-185
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• 2008

Accumulating evidence has suggested the existence of reciprocal communication between immune, endocrine, and neurotransmitter system. Cytokine hypothesis of depression implies that increased pro-inflammatory cytokine such as -1, IL-6, IL-12, TNF-${\alpha}$, and IFN-${\gamma}$ in major depression, acting neuromodulators, play a key role in the mediation of behavioral, neuroendocrine, and neurochemical disturbances in depression. Concerning the relation between cytokines and serotonin metabolism, pro-inflammatory cytokines have profound effects on the metabolism of brain serotonin through the enzyme indoleamine-2,3-dioxygenase(IDO) that metabolizes tryptophan, the precursor of 5-HT to neurodegenerative quinolinate and neuroprotective kynurenate. The neurodegeneration process is reinforced by the neurotoxic effect of the hypercortisolemia during depression. From this perspective, it is possible that efficacy of antidepressants in the treatment of depression may, at least in part, rely on downregulation of pro-inflammatory cytokine synthesis. So, the use of cytokine synthesis inhibitors or cytokine antagonists may be a new treatment approach in depression. However, at present the question whether cytokines play a causal role in the onset of depression or are mere epiphenomena sustaining depressive symptoms remains to be elucidated. Nevertheless, cytokine hypothesis has created new perspectives in the study of psychological and pathophysiological mechanism that are associated with major depression, as well as the prospect for developing a new generation antidepressants.

• The Journal of Korean Physical Therapy
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• v.13 no.1
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• pp.219-227
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• 2001

Capsaicin. a vanillyl amide(8-methy1-N-vanilly1-6-nonenamide) with a molecular weight of 305.42, was substance, interrupting the pain conducting pathway Until recently the neurotoxic effects of Capsaicin to adult animals were thought to be limited to the peripheral nervous system. But several reports suggest the possibility of central nervous system changes after Capsaicin administration to the adult rat. Capsaicin desensitization is defined as long lasting, reversible suppression of sensory neuron activity. How fast and for how long the desensitization develops is related to the dose and time of exposure to Capsaicin, and the interval between consecutive dosing. In the long term Capsaicin treatment can lead to morphological degeneration and changes in some small sensory neurons, predominantly unmyelinated C fiber afferent nerve fibers. Clinical interest has recently been roused by evidence that Capsaicin's desensitizing action may be of therapeutic value and that an endogenous Capsaicin-1 ike substance may exist. This study summarizes the fundamental knowledge(mechanism, receptors, et al of Capsaicin) of Capsaicin for physical therapists.

• Journal of Physiology & Pathology in Korean Medicine
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• v.30 no.1
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• pp.33-39
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• 2016

Alzheimer's disease(AD), one of the most common forms of dementia, is characterized pathologically by the presence of intracellular neurofibrillary tangles and deposition of β-amyloid(Aβ) peptides of 40-42 residues. Aβ has been believed to be neurotoxic and now is also considered to have a role on the mechanism of memory dysfunction. Only a few acetylcholinesterase(AChE) inhibitors have been developed for treatment of AD, although the numbers of patients are rapidly increasing within aging society. Here, we show that ethanol extract of Rosae Rugosae Flos(RR) or its butanol fraction reduce the enzyme activity of AChE and BACE1(β-site APP cleaving enzyme 1). Furthermore, We found that RR inhibits Aβ aggregation and removes Aβ aggregates by Transmission electron microscopy(TEM). In addition, RR reduces the free radical of 2, 2-diphenyl-1-picrylhydrazyl(DPPH). We suggest that Rosae Rugosae Flos may be useful as a herbal medicine to treat AD.