• Journal of Yeungnam Medical Science
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• v.30 no.1
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• pp.4-9
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• 2013

Leptin, a 16-kDa cytokine, is secreted by adipose tissue in response to the surplus of fat store. Thereby, the brain is informed about the body's energy status. In the hypothalamus, leptin triggers specific neuronal subpopulations (e.g., POMC and NPY neurons) and activates several intracellular signaling events, including the JAK/STAT, MAPK, PI3K, and mTOR pathway, which eventually translates into decreased food intake and increased energy expenditure. Leptin signal is inhibited by a feedback inhibitory pathway mediated by SOCS3. PTP1B involves another inhibitory pathway of leptin. Leptin potently promotes fat mass loss and body weight reduction in lean subjects. However, it is not widely used in the clinical field because of leptin resistance, which is a common feature of obesity characterized by hyperleptinemia and the failure of exogenous leptin administration to provide therapeutic benefit in rodents and humans. The potential mechanisms of leptin resistance include the following: 1) increases in circulating leptin-binding proteins, 2) reduced transport of leptin across the blood-brain barrier, 3) decreased leptin receptor-B (LRB), and/or 4) the provocation of processes that diminish cellular leptin signaling (inflammation, endoplasmic reticulum stress, feedback inhibition, etc.). Thus, interference of the cellular mechanisms that attenuate leptin signaling improves leptin action in cells and animal models, suggesting the potential utility of these processes as points of therapeutic intervention. Various experimental trials and compounds that improve leptin resistance are introduced in this paper.

• Korean Journal of Biological Psychiatry
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• v.5 no.2
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• pp.219-226
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• 1998

Cytosine arabinoside(AraC) inhibits DNA synthesis and ${\beta}$-DNA polymerase, an enzyme involved in DNA repair. This, a potent antimitotic agent, is clinically used as an anticancer drug with side effect of severe neurotoxicity. Earlier reports suggested that inhibition of neuronal survival by AraC in sympathetic neuron may be due to the inhibition of a 2'-deoxycytidine-dependent process that is independent of DNA synthesis or repair and AraC induced a signal that is triggers a cascade of new mRNA and protein synthesis, leading to apoptotic cell death in cultured cerebellar granule cells. The present study would suggest whether caspase family(ICE/CED-3-like protease) involved in AraC-induced apoptosis pathway of PC12 cells. It was observed that treatment of PC12 cells with AraC led to decrease of viability by MTT assay and morphology changes, which did not suggest that AraC induced apoptosis in PC12 cells. The mRNA of caspase-1/caspase-3 were expressed in PC12 cells constitutively, and AraC did not activate caspase family. These results suggest that caspase-1/caspase-3 may not be required for AraC-induced cell death pathway in PC12 cells.

• BMB Reports
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• v.31 no.2
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• pp.117-122
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• 1998

Changes of lipocortin 1 (LC1) in the brain induced by immobilization stress were investigated in rats. Rats were immobilized for 0,1,2,3,4, and 5 h, and the brain slices were immunostained with anti-human LC1 antibodl (anti-LC1). Immunoreactivity of LCI (iLC1) was most prominent in neuronal cell bodies and processes of hippocampal CA regions and dentate gyrus. At rest without stress, most of the LC1 in the neuron located in the cytoplasm with the nuclei exhibiting relatively scarce immunoreactivity. Immobilization stress changed this intracellular distribution of LC1 by increasing nuclear LC1. The change was apparent in 1 h and reached the peak by 3 h. However, by 5 h of immobilization, the distribution pattern returned to that of the resting state. This transient nuclear translocation of LC1 was most prominent in $CA_1$ pyramidal neurons, and was not observed in areas other than the hippocampus. Adrenalectomy abolished this transient translocation of LC1. The roles of hippocampal LC1 as a mediator of glucocorticoid feedback signal and/or as an intracellar stress signaling protein could be suggested.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.10a
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• pp.176-176
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• 2003

Methylmercury is known to have devastating effects on the mammalian nervous system. When human neuroblastoma SH-SY5Y cells were treated with methylmercury at sublethal concentrations (6.25 uM), up-regulated genes (39) ＆ down-regulated genes (19) were identified by human 8k cDNA microarray. These genes are related with microtubule process, signal transduction pathway and cell death (apoptosis), Apoptosis-associated genes, HSP70, CDK inhibitor 1, FOS-like antigen were up-regulated and microtubule related genes like villin and dynein down-regultaed. To confirm the presence of apoptosis in cultured SH-SY5Y cells treated 6.25 and 1 uM methylmercury, we applied Annexin V-FITC assay followed by flow cytometric measurements after 6 and 24h. Studies on transcriptional and molecular effect by methylmercury may provide an insight into the neurotoxic effects of methylmercury in human neuronal cells and a possibility to develop more efficient and exact monitoring system of heavy metals as ubiquitous environmental pollutants.

• Natural Product Sciences
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• v.15 no.1
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• pp.32-36
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• 2009

Glutamate causes neurotoxicity through formation of reactive oxygen species and activation of mitogen-activated protein kinase (MAPK) pathways. MAPK phosphatase-1 (MKP-1) is one of the phosphatases responsible for dephosphorylation/deactivation of three MAPK families: the extracellular signal-regulated kinase-1/2 (ERK-1/2), the c-Jun N-terminal kinase-1/2 (JNK-1/2), and the p38 MAPK. In this report, the potential involvement of MKP-1 in neuroprotective effects of curcumin, the active ingredient of turmeric (Curcuma longa), was examined using HT22 cells. Glutamate caused cell death and activation of ERK-1/2 but not p38 MAPK or JNK-1/2. Blockage of ERK-1/2 by its inhibitor protected HT22 cells against glutamate-induced toxicity. Curcumin attenuated glutamate-induced cell death and ERK-1/2 activation. Interestingly, curcumin induced MKP-1 activation. In HT22 cells transiently transfected with small interfering RNA against MKP-1, curcumin failed to inhibit glutamate-induced ERK-1/2 activation and to protect HT22 cells from glutamate-induced toxicity. These results suggest that curcumin can attenuate glutamate-induced neurotoxicity by activating MKP-1 which acts as the negative regulator of ERK-1/2. This novel pathway may contribute to and explain at least one of the neuroprotective actions of curcumin.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.2
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• pp.431-437
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• 2008

Sengmaek-san(Shengmai-san; SMS) is used in oriental medicine as one of the key herbal medicine for treating diverse symptoms including cardiovascular and neurological disorders. In the present study, the effects of SMS on axonal regeneration were investigated in the rat model given sciatic nerve injury. SMS treatment enhanced axonal regrowth into and the number of non-neuronal cells in the distal area after crush injury. GAP-43 protein levels were increased in the injured sciatic nerve compared to intact nerve and further upreguated by SMS treatment. GAP-43 protein was increased similarly in the dorsal root ganglion (DRG) at lumbar 4 - 6 by nerve injury and SMS treatment, suggesting GAP-43 induction at gene expression level. SMS-mediated increase in phospho-Erk1/2 protein was observed in the DRG as well as in the injured nerve implying its retrograde transport into the cell body as the process of lesion signal transmission. The present findings suggest that SMS may be involved in enhanced axonal regeneration via dynamic regulation of regeneration-associated proteins.

• Journal of Haehwa Medicine
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• v.10 no.1
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• pp.365-374
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• 2001

The brain is one of the most complex systems in nature. Brain waves, or the "EEG", are electrical signals that can be recorded from the brain, either directly or through the scalp. The kind of brain wave recorded depends on the behavior of the animal, and is the visible evidence of the kind of neuronal (brain cell) processing necessary for that behavior. But, EEG had been considered as a virtually infinite-dimensional random signal. However, nonlinear dynamics light on dynamical aspects of the human EEG. The methods of nonlinear dynamics provide excellent tolls for the study of multi-variable, complex system such as EEG. In this study, 20 persons seperated in 2 groups were examined with EEG, one group stimulated on specific area of the sole of the foot with footbed inside the shoes. This experiment resulted in at the group stimulated on specific area of the sole of the foot correlation dimension of P4 and O1 channels increased significantly. Therefore. we obserbed that stimulation on specific area of the body had a constant effections on the specific channels.

• Journal of Fashion Business
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• v.16 no.2
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• pp.124-137
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• 2012

This study aims to identify the meaning and formation cause of a style, and the essential elements of style formation, through psychobiological research as well as an analysis of the designs of Iris Van Herpen, a fashion designer, who in just 6 years has developed into a world-renowned new designer. As a result, it has been found that the psychobiological causes to form a style stem from the action of 'long-term memory', which is consolidated by 'selective attention', 'perceptional subjectivity', the principle of the 'neuron's connection specificity and invariance', and the principle of a 'neuronal signal's unilateral flow'. With such action, Herpen could develop her own original composition techniques. The formative shapes created by such composition techniques are characterized by enumeration, superposition, and hanging. The study has also found that the essential elements for a designer to be able to form his/her own style include 'aesthetic originality' in which the designer views the property of a thing from his/her inherent perspective, and finds the uniqueness from the thing that only he/she can express, 'technical differences' that are creative and original, and 'formative specificity' that is summarized into one property through an impressive shape.

• Journal of Ginseng Research
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• v.43 no.2
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• pp.163-171
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• 2019

Common features of neurodegenerative diseases (NDDs) include progressive dysfunctions and neuronal injuries leading to deterioration in normal brain functions. At present, ginseng is one of the most frequently used natural products. Its use has a long history as a cure for various diseases because its extracts and active compounds exhibit several pharmacological properties against several disorders. However, the pathophysiology of NDDs is not fully clear, but researchers have found that various ion channels and specific signaling pathways might have contributed to the disease pathogenesis. Apart from the different pharmacological potentials, ginseng and its active compounds modulate various ion channels and specific molecular signaling pathways related to the nervous system. Here, we discuss the signal modulating potential of ginseng and its active compounds mainly focusing on those relevant to NDDs.

• Molecules and Cells
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• v.45 no.4
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• pp.231-242
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• 2022

The neuromuscular junction (NMJ), which is a synapse for signal transmission from motor neurons to muscle cells, has emerged as an important region because of its association with several peripheral neuropathies. In particular, mutations in GARS that affect the formation of NMJ result in Charcot-Marie-Tooth disease and distal hereditary motor neuropathy. These disorders are mainly considered to be caused by neuronal axon abnormalities; however, no treatment is currently available. Therefore, in order to determine whether the NMJ could be targeted to treat neurodegenerative disorders, we investigated the NMJ recovery effect of HDAC6 inhibitors, which have been used in the treatment of several peripheral neuropathies. In the present study, we demonstrated that HDAC6 inhibition was sufficient to enhance movement by restoring NMJ impairments observed in a zebrafish disease model. We found that CKD-504, a novel HDAC6 inhibitor, was effective in repairing NMJ defects, suggesting that treatment of neurodegenerative diseases via NMJ targeting is possible.