• Biomolecules & Therapeutics
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• v.13 no.2
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• pp.84-89
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• 2005

The purpose of this study was to characterize the putative anxiolytic-like effects of the aqueous extract of the root of Polygala tenuifolia ( AEPT) using an elevated plus maze (EPM) and hole-board apparatus in mice. The AFPT was orally administered at 50, 100, 200 or 400 mg/kg to ICR mice, 1 h before the behavioral evaluation in the EPM respectively. Control mice were treated with an equal volume of saline, and positive control mice with buspirone (2 mg/kg). Single treatments of the AEPT significantly increased the percentage of time spent and arm entries into the open arms of the EPM vedrsus saline controls (P<0.05). Moreover, there were no changes in the locomotor activity and myorelaxant effects in any group compared with the saline controls. In the hole-board test,single treatments of the AEPT (200 and 400 mg/kg) significantly increased the number of headdips versus saline controls (P<0.05). In addition, the anxiolytic-like effects of the AEPT were blocked by WAY 100635(0.3mg/kg, I.p), a5-$HT_{1A}$ receptor antagonist not by flumazenil, a $GABA_{A}$ antagonist. These results indicate that P. tenuifolia is an effective anxiolytic agent, andsuggest that the anxiolytic-like effects of P. tenuifolia is mediated via the serotonergic nervous system.

• Journal of Acupuncture Research
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• v.22 no.3
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• pp.37-51
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• 2005

Mast cell is a cell that functions mainly in our body with a respect to inflammation and allergic response. Bee venom has been progressed in a study as a model related to mechanism in alleviation of pain until now, but it is being progressed in a study relevant to immunocyte in anti-inflammation or anti-allergic response. The present study is aimed to present the basis related to a future study of gene, by researching the influence of melittin and MCD Peptide, which are major ingredients in Bee venom, upon the expression of gene in the mast cell strain. In this study, it dealt with melittin and MCD Peptide respectively, in the effective concentration after passing though the experiment of cytotoxicity by using human mast cell strain. Also, with the respect in the aspect of expression in gene that changes at this time, information was obtained through the technique of analyzing microarray. Through experimental statistics, when regarding a case that global M is significant in more than 1 or -1, in melittin, all 7 genes were accelerated, and 8 inhibited. In MCDP, 7 genes were accelerated and 17 genes inhibited. The function in the body to which these genes are related, was associated with the protein binding within a cell, the activation in the function of lymphocyte, the acceptor related to macrophage antigen. In cell nucleus, substance related to GABA A receptor, protein associated with cAMP reactive element, substance related to complement system No.8 and to B-cell, protein substance related to polycystic kidney disease, substance related to inflammation, and the protein substance of influencing coagulation of blood. Through these results of analysis, it could obtain more useful materials in clarifying the mechanism of action in melittin and MCD peptide, which are in charge of mainly medical action in the abdomen. Also, it is thought that an in-depth study on the influence of main ingredients in Bee venom, the wholly honey bee venom aqua upon anti-allergic response or anti-inflammation are further required.

• Journal of Pharmacopuncture
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• v.15 no.3
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• pp.19-30
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• 2012

Objectives: Many efforts have shown multi-oncologic roles of galectin-3 for cell proliferation, angiogenesis, and apoptosis. However, the mechanisms by which galectin-3 is involved in cell proliferation are not yet fully understood, especially in human colon cancer cells. Methods: To cluster genes showing positively or negatively correlated expression with galectin-3, we employed human colon cancer cell lines, SNU-61, SNU-81, SNU-769B, SNU-C4 and SNU-C5 in high-throughput gene expression profiling. Gene and protein expression levels were determined by using real-time quantitative polymerase chain reaction (PCR) and western blot analysis, respectively. The proliferation rate of human colon cancer cells was measured by using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Results: Expression of ${\gamma}$-aminobutyric acid B receptor 1 (GABABR1) showed a positive correlation with galectin-3 at both the transcriptional and the translational levels. Down-regulation of galectin-3 decreased not only GABABR1 expression but also the proliferation rate of human colon cancer cells. However, Korean herbal extract, HangAmDan-B (HAD-B), decreased expression of GABABR1 without any expressional change of galectin-3, and offset ${\gamma}$-aminobutyric acid (GABA)-enhanced human colon cancer cell proliferation. Conclusions: Our present study confirmed that GABABR1 expression was regulated by galectin-3. HAD-B induced galectin-3-independent down-regulation of GABABR1, which resulted in a decreased proliferation of human colon cancer cells. The therapeutic effect of HAD-B for the treatment of human colon cancer needs to be further validated.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.6
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• pp.996-999
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• 2011

This experiment was performed to investigate whether the combined-preparation of crude drugs (The $Well^{TM}$ Preparation, TW), has hypnotic effects and/or enhances pentobarbital-induced sleep behaviors. TW was mixed with water extracts of Ginseng Radix red, Germinated brown rice, cultured mountain ginseng, and 50% ethanol extracts of Longanae Arillus, Nelumbinis Folium and Chrysanthemi Flos. TW (100 mg/kg, p.o.) reduced sleep onset and prolonged sleep time induced by pentobarbital similar to muscimol (0.2 ${\mu}M$), a $GABA_A$ receptor agonist. Also, TW (2 ${\mu}g$/ml) and pentobarbital (2.5 ${\mu}M$) did not affect the chloride influx in primary cultured cerebellar granule cells, respectively, but the combined-treatment of TW (2 ${\mu}g$/ml) and pentobarbital (2.5 ${\mu}M$) increased the chloride influx onto the cells. In conclusion, TW augments pentobarbital-induced sleep behaviors; these effects may result from chloride channel activation.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.3-19
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• 2001

Recent basic and clinical studies demonstrate a major role for neural plasticity in the etiology and treatment of depression and stress-related illness. The neural plasticity is reflected both in the birth of new cell in the adult brain(neurogenesis) and the death of genetically healthy cells(apoptosis) in the response to the individual's interaction with the environment. The neural plasticity includes adaptations of intracellular signal transduction pathway and gene expression, as well as alterations in neuronal morphology and cell survival. At the cellular level, repeated stress causes shortening and debranching of dendrite in the CA3 region of hippocampus and suppress neurogenesis of dentate gyrus granule neurons. At the molecular level, both form of structural remodeling appear to be mediated by glucocorticoid hormone working in concert with glutamate and N-methyl-D-aspartate(NMDA) receptor, along with transmitters such as serotonin and GABA-benzodiazepine system. In addition, the decreased expression and reduced level of brain-derived neurotrophic factor(BDNF) could contribute the atrophy and decreased function of stress-vulnerable hippocampal neurons. It is also suggested that atrophy and death of neurons in the hippocampus, as well as prefrontal cortex and possibly other regions, could contribute to the pathophysiology of depression. Antidepressant treatment could oppose these adverse cellular effects, which may be regarded as a loss of neural plasticity, by blocking or reversing the atrophy of hippocampal neurons and by increasing cell survival and function via up-regulation of cyclic adenosine monophosphate response element-binding proteins(CREB) and BDNF. In this article, the molecular and cellular mechanisms that underlie stress, depression, and action of antidepressant are precisely discussed.

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.1
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• pp.37-44
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• 1997

The Purpose of this study was to evaluate the effect of cooking methods and reheating on texture characteristics of sausage. Sausage samples were cooked(microwaving, gas-broiling and frying), reheated on day 3 and 6 after refrigeration and put to evaluation of sensory and texture characteristics. The results of sensory evaluation showed that hardness, salty taste, rancid flavor and after-taste were increased but wetness and chewiness were decreased by reheating after refrigeration. Overall acceptability was the highest when the samples were gas broiled and reheated on day 3 after refrigeration. As for the estimation of texture changes by rheometer, hardness, cohesiveness, elasticity, gum-miness and chewiness tended to increase by reheating after refrigeration. Hardness, cohesiveness, gumminess and chewiness were the highest when the samples were gas-broiled and reheated on day 3 after refrigeration.

• Nutrition Research and Practice
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• v.12 no.3
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• pp.199-207
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• 2018

BACKGROUND/OBJECTIVES: Fermented Laminaria japonica (FL), a type sea tangle used as a functional food ingredient, has been reported to possess cognitive improving properties that may aid in the treatment of common neurodegenerative disorders, such as dementia. MATERIALS/METHODS: We examined the effects of FL on scopolamine (Sco)- and ethanol (EtOH)-induced hippocampus-dependent memory impairment, using the Passive avoidance (PA) and Morris water maze (MWM) tests. To examine the underlying mechanisms associated with neuroprotective effects, we analyzed acetylcholine (ACh) and acetylcholinesterase (AChE) activity, brain tissue expression of muscarinic acetylcholine receptor (mAChR), cAMP response element binding protein (CREB) and extracellular signal-regulated kinases 1/2 (ERK1/2), and immunohistochemical analysis, in the hippocampus of mice, compared to current drug therapy intervention. Biochemical blood analysis was carried out to determine the effects of FL on alanine transaminase (ALT), aspartate transaminase (AST), and triglyceride (TG) and total cholesterol (TC) levels. 7 groups (n = 10) consisted of a control (CON), 3 Sco-induced dementia and 3 EtOH-induced dementia groups, with both dementia group types containing an untreated group (Sco and EtOH); a positive control, orally administered donepezil (Dpz) (4mg/kg) (Sco + Dpz and EtOH + Dpz); and an FL (50 mg/kg) treatment group (Sco + FL50 and EtOH + FL50), orally administered over the 4-week experimental period. RESULTS: FL50 significantly reduced EtOH-induced increase in AST and ALT levels. FL50 treatment reduced EtOH-impaired step-through latency time in the PA test, and Sco- and EtOH-induced dementia escape latency times in the MWM test. Moreover, anticholinergic effects of Sco and EtOH on the brain were reversed by FL50, through the attenuation of AChE activity and elevation of ACh concentration. FL50 elevated ERK1/2 protein expression and increased p-CREB (ser133) in hippocampus brain tissue, according to Western blot and immunohistochemistry analysis, respectively. CONCLUSION: Overall, these results suggest that FL may be considered an efficacious intervention for Sco- and EtOH-induced dementia, in terms of reversing cognitive impairment and neuroplastic dysfunction.

• Applied Microscopy
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• v.41 no.4
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• pp.235-248
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• 2011

Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adults and is a major risk factor for the development of posttraumatic epilepsy (PTE). Recent studies have provided significant insight into the pathophysiological mechanisms underlying the development of epilepsy. Although the link between brain trauma and epilepsy is well recognized, the complex biological mechanisms that result in PTE following TBI have not been fully elucidated. Therefore, this study investigated in order to identify whether or not the abnormal expression of calcium-binding proteins in the lesioned hippocampus plays a role in neuronal damage by brain trauma and whether or not the expressions may change in the contralateral hippocampus during the adaptive stage as early time point following TBI. During early time point following TBI, both parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities were decreased with in the lesioned hippocampus. However, these expressions were recovered to control levels as depend on time courses. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced as compared to the control levels, whereas CB expression was unchanged. These findings indicate that the alterations of the calcium-binding proteins, especially PV and CB, may contribute to the neuronal death and/or damage induced by abnormal inhibitory neurotransmission at early time period following brain trauma and the development of epileptogenesis in patients with traumatic brain injury.