• Korean Journal of Food Science and Technology
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• v.49 no.5
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• pp.550-558
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• 2017

The effect of Artemisia argyi H. under liquid-state fermentation by Monascus purpureus (AAFM) on cognitive impairments has been studied in a mice model of diabetes-associated cognitive decline induced by streptozotocin (STZ). C57BL/6 mice (9 weeks of age, male) were separated into four groups: a normal control, STZ-induced diabetic mouse group (STZ group), Artemisia argyi H. (AA) 10 group (diabetic mouse+AA 10 mg/kg/day), AAFM 10 group (diabetic mouse+AAFM 10 mg/kg/day). Administration of AA and AAFM significantly improved glucose tolerance, as shown by the intraperitoneal glucose tolerance test (IPGTT), and ameliorated cognitive deficit, as shown by the behavioral tests including passive avoidance, Morris water maze, and Y-maze tests. After behavioral tests, the cholinergic system was examined by assessment of the acetylcholine (ACh) level and acetylcholinesterase (AChE) inhibitory activity, and the antioxidant system was also assessed by measuring malondialdehyde (MDA) and superoxide dismutase (SOD) levels in the brain and liver.

• Food Science of Animal Resources
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• v.33 no.2
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• pp.258-267
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• 2013

This study was conducted to determine the antioxidative and neuroprotective effect of pig skin extracts (PS) and pig skin gelatin hydrolysates (LPS) using a human neuroblastoma cell line (SH-SY5Y). The extraction yield of PS was 3 fold higher than that of LPS. The protein content of PS was about 10 fold higher than that of LPS (p<0.05). Also LPS increased antioxidative activity dose dependently, and the activity was significantly higher than PS at all concentration (p<0.05). DPPH radical scavenging activity of LPS at 50 mg/mL was 92.97%, which was similar to $1{\mu}M$ vitamin C as a positive control. ABTS radical scavenging activity of LPS (20 mg/mL) was 89.83% and oxygen radical absorbance capacity of LPS at 1 mg/mL was $141.39{\mu}M$ Trolox Equvalent/g. No significant change of human neuroblastoma cells was determined by MTT test. Cell death by oxidative stress induced by $H_2O_2$ and amyloid beta 1-42 ($A{\beta}_{1-42}$) was protected by LPS rather than PS. Acetylcholine esterase was significantly inhibited, by up to 33.62% by LPS at 10 mg/mL. Therefore, these results suggest that pig skin gelatin hydrolysates below 3 kDa have potential to be used as anti-oxidative and neuroprotective functional additives in the food industry, while further animal test should be determined in the future.

• Journal of the Korean Applied Science and Technology
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• v.37 no.3
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• pp.448-462
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• 2020

Dietary nutrition is a critical lifestyle factor that can reduce the risk of future cognitive impairments caused by dementia. Accumulating evidence suggests that dietary supplementation with Sulforaphane may help the prevention of cognitive impairments and dementia. Thus, Sulforaphane-enriched broccoli extract would hold promise to improve cognitive impairments of dementia patients. Here, we have used broccoli extracts, prepared from broccoli cultivated in Magma Seawater, to test if the broccoli extracts can be dietary supplement to improve cognitive impairments. Magma Seawater originated from Jeju Island, Korea is unique in terms of containing high concentrations of usable minerals (Zinc, Vanadium and Germanium etc.). Broccoli, grown in Magma Seawater, would contain Sulforaphane and the extra amount of usable minerals. The chemical compositions of the broccoli extracts were analyzed using LC-Q-orbitrap to detect Sulforaphane and Glucoraphanin. Analysis method based on HPLC was developed for measurement of sulforaphane levels in the broccoli extracts. We have tested if the broccoli extracts have anti-apoptotic and anti-inflammatory effects on neuron-like SH-SY5Y cells. In addition, we examined if the broccoli extracts are able to upregulate expression of synaptic plasticity-associated proteins (BDNF and phospho-CREB) and to inhibit acetylcholine esterase (AchE) activity. We have shown that the broccoli extracts inhibited the apoptotic pathway and inflammatory responses. Finally, we present evidence showing that AchE activity was inhibited by the broccoli extracts, but expression of BDNF and phospho-CREB was upregulated. Taken together, these findings suggest that the broccoli extracts from Magma Seawater-grown broccoli would be a good source of dietary nutrition to improve cognitive impairments in the future.

• The Journal of Internal Korean Medicine
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• v.18 no.2
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• pp.1-26
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• 1997

Chunggeumtang has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Chunggeumtang on tracheal smooth muscle is not konwn. The purpose of the present study is to determine the effect of Chunggeumtang on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig(500g, male) and Sprague Dawley rats (250g, male) were killed by $CO_2$ exposure and a segment (8-10mm) of the thoracic trachea from each rat and guinea pig was cut into equal swegments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force diplacement transducers under 0.5g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response ($ED_{50}$) was obtained from cumulative dose response curves for histamine and acetylcholine($10^{-7}{\sim}10^{-4}M$). Contractions evoked by His ($ED_{50}$) and Ach ($ED_{50}$) were inhibited significantly by Chunggeumtang. In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $6.1%after\;30{\mu}l/ml$ Chunggeumtang, and 49.4% (p<0.01) after $100{\mu}l/ml$ Chunggeumtang. In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $6.7%\;after\;30{\mu}l/ml$ Chunggeumtang, and $54.2%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $30.6%\;(p<0.05)\;after\;30{\mu}l/ml$ Chunggeumtang, and $53.0%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $24.1%\;(p<0.05)\;after\;30{\mu}l/ml$ Chunggeumtang, and $55.3%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. Propranolol and indomethacin($10^{-7}M$) slightly but significantly attenuated the inhibitory effects of Chunggeumtang. Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 27.6% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 28.7% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 16.2% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 28.7% (p<0.05) in rat induced by histamine contraction. Indomethacin, the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 20.0% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 16.9% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 16.4% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 23.1% (p<0.05) in rat induced by histamine contraction. Methylene blue($10^{-7}M$) did not significantly alter the inhibitory effect of Chunggeumtang. Also, I could find the effects of Chunggeumtang and Chunggeumtanggamorphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Chunggeumtang can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects and the release of cyclooxygenase products.

• Korean Journal of Environmental Agriculture
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• v.37 no.4
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• pp.268-276
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• 2018

BACKGROUND: In the month of January 2018, fine dust alerts and warnings were issued 36 times for $PM_{10}$ and 81 times for PM2.5. Air quality is becoming a serious issue nation-wide. Although interest in air-purifying plants is growing due to the controversy over the risk of chemical substances of regular air-purifying solutions, industrial spread of the plants has been limited due to their efficiency in air-conditioning perspective. METHODS AND RESULTS: This study aims to propose a vegetation-based bio-filter system that can assure total indoor air volume for the efficient application of air-purifying plants. In order to evaluate the quantitative performance of the system, time-series analysis was conducted on air-conditioning performance, indoor air quality, and comfort index improvement effects in a lecture room-style laboratory with 16 persons present in the room. The system provided 4.24 ACH ventilation rate and reduced indoor temperature by $1.6^{\circ}C$ and black bulb temperature by $1.0^{\circ}C$. Relative humidity increased by 24.4% and deteriorated comfort index. However, this seemed to be offset by turbulent flow created from the operation of air blowers. While $PM_{10}$ was reduced by 39.5% to $22.11{\mu}g/m^3$, $CO_2$ increased up to 1,329ppm. It is interpreted that released $CO_2$ could not be processed because light compensation point was not reached. As for the indoor comfort index, PMV was reduced by 83.6 % and PPD was reduced by 47.0% on average, indicating that indoor space in a comfort range could be created by operating vegetation-based bio-filters. CONCLUSION: The study confirmed that the vegetation-based bio-filter system is effective in lowering indoor temperature and $PM_{10}$ and has positive effects on creating comfortable indoor space in terms of PMV and PPD.

• Journal of agriculture & life science
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• v.50 no.2
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• pp.125-138
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• 2016

To assess the industrial possibility of mixed-extracts containing Hovenia dulcis Thunberg and 12 different botanical ingredients, a protective effect was confirmed in the chronic ethanol-induced the liver, brain, and blood injury in mouse. Blood glucose levels of the normal control group(NG) and ethanol administration group(EG) were respectively 119.43mg/dL and 305.25mg/dL, and the mixed-extracts administration group(100, 200mg/kg body weight + 25% ethanol 5g/kg body weight respectively; ME100 & ME200) were decreased to 272.76mg/dL and 234.60mg/dL. Blood ethanol contents were decreased in ME100 and ME200(3.85mg/dL, 3.08mg/dL) compared to EG(4.08mg/dL), and blood acetaldehyde contents were also decreased in ME(15.76mg/dL, 15.16mg/dL) compared to EG(18.72mg/dL). The contents of hepatotoxic indicators such as glutamine pyruvic transaminase(GPT) and glutamic oxaloacetic transaminase (GOT), nephrotoxic indicators such as blood urea nitrogen(BUN), and creatine(CRE), and total cholestero(TCHO), and triglyceride(TG) in mouse blood serum were significantly decreased in the ME compared to EG. The acetylcholinesterase(AChE) activity of ME(109.00% and 108.47%, respectively) in mouse brain tissues was decreased in ME compared to EG(116.10%). Finally, ME was remarkable in vivo antioxidant activities in the mouse liver and brain tissues by superoxide dismutase(SOD), oxidized glutathione(GSH)/total GSH ratio and the malondialdehyde (MDA) assay. Therefore, the mixed-extracts was considered to be effective a high value food with protective effect against chronic ethanol traetment-induced cytotoxicity in liver and brain tissues.

• Molecules and Cells
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• v.38 no.9
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• pp.796-805
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• 2015

Gintonin is a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand. Oral administration of gintonin ameliorates learning and memory dysfunctions in Alzheimer's disease (AD) animal models. The brain cholinergic system plays a key role in cognitive functions. The brains of AD patients show a reduction in acetylcholine concentration caused by cholinergic system impairments. However, little is known about the role of LPA in the cholinergic system. In this study, we used gintonin to investigate the effect of LPA receptor activation on the cholinergic system in vitro and in vivo using wild-type and AD animal models. Gintonin induced $[Ca^{2+}]_i $ transient in cultured mouse hippocampal neural progenitor cells (NPCs). Gintonin-mediated $[Ca^{2+}]_i $ transients were linked to stimulation of acetylcholine release through LPA receptor activation. Oral administration of gintonin-enriched fraction (25, 50, or 100 mg/kg, 3 weeks) significantly attenuated scopolamine-induced memory impairment. Oral administration of gintonin (25 or 50 mg/kg, 1 2 weeks) also significantly attenuated amyloid-${\beta}$ protein ($A{\beta}$)-induced cholinergic dysfunctions, such as decreased acetylcholine concentration, decreased choline acetyltransferase (ChAT) activity and immunoreactivity, and increased acetylcholine esterase (AChE) activity. In a transgenic AD mouse model, long-term oral administration of gintonin (25 or 50 mg/kg, 3 months) also attenuated AD-related cholinergic impairments. In this study, we showed that activation of G protein-coupled LPA receptors by gintonin is coupled to the regulation of cholinergic functions. Furthermore, this study showed that gintonin could be a novel agent for the restoration of cholinergic system damages due to $A{\beta}$ and could be utilized for AD prevention or therapy.

• Journal of Life Science
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• v.25 no.10
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• pp.1103-1109
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• 2015

Cholinergic innervation of the hippocampus is known to be correlated with learning and memory. The cholinergic agonist carbachol (CCh) modulate synaptic plasticity and produced long-term synaptic depression (LTD) in the hippocampus. However, the exact mechanisms by which the cholinergic system modifies synaptic functions in the hippocampus have yet to be determined. This study introduces an acetylcholine receptor-mediated LTD that requires internalization of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors on the postsynaptic surface and their intracellular mechanism in the hippocampus. In the present study, we showed that the application of the cholinergic agonist CCh reduced the surface expression of GluA2 on synapses and that this reduction was prevented by the M1 muscarinic acetylcholine receptor antagonist pirenzepine in primary hippocampal neurons. The interaction between GluA2 and the glutamate receptor-interacting protein 1 (GRIP1) was disrupted in a hippocampal slice from a rat upon CCh simulation. Under the same conditions, the binding of GluA2 to adaptin-α, a protein involved in clathrin-mediated endocytosis, was enhanced. The current data suggest that the activation of LTD, mediated by the acetylcholine receptor, requires the internalization of the GluA2 subunits of AMPA receptors and that this may be controlled by the disruption of GRIP1 in the PDZ ligand domain of GluA2. Therefore, we can hypothesize that one mechanism underlying the LTD mediated by the M1 mAChR is the internalization of the GluA2 AMPAR subunits from the plasma membrane in the hippocampal cholinergic system.

• Korean Journal of Food Science and Technology
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• v.49 no.2
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• pp.222-227
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• 2017

Red ginseng prepared from fresh 6-year-old ginseng treated with colloidal gold nanoparticles was extracted using hot water to evaluate its total phenolic and flavonoid contents, antioxidant capacity, and neuroprotective effects. Water extract of red ginseng treated with gold nanoparticles (WERGGN) had total phenolic and total flavonoid contents of 212.2 mg gallic acid equivalents/$^{\circ}Bx$ and 3.5 mg catechin equivalents/$^{\circ}Bx$, respectively. The antioxidant capacities of WERGGN measured using ABTS, DPPH, and ORAC assays were 272.3, 141.2, and 868.4 mg vitamin C equivalents/$^{\circ}Bx$, respectively. The WERGGN showed protective effects on the viability of neuron-like PC-12 cells against oxidative stress induced by hydrogen peroxide in a dose-dependent manner, partly because of a reduction in intracellular oxidative stress. Acetylcholinesterase and butyrylcholinesterase, which degrade the neurotransmitter acetylcholine to terminate neurotransmission, were inhibited by treatment with WERGGN. These results suggest that WERGGN is useful as a functional material to decrease oxidative stress and neuronal damage.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.181-190
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• 1994

Endothelium-derived relaxing factor (EDRF) activates guanylate cyclase which mediates the formation of cGMP from GTP in vascular smooth muscle. It is well known that endothelium-dependent relaxation is impaired in spontaneously hypertensive rats (SHR). However, it is still unknown whether the impaired endothelium-dependent relaxation in SHR results from the reduced release of EDRF or from the decrease of vascular response to EDRF. We investigated the effects of cGMP on the contractility and Ca movement in the aorta of SHR and Wistar-Kyoto rats (WKY). The amplitude of the endothelium-dependent relaxation to actylcholine (ACh) was significantly less in SHR than in WKY. L-arginine $(10^{-3}M)$ did not increase endothelium-dependent relaxation in both strains. Sodium nitroprusside (SNP), an activator of guanylate cyclase, relaxed the 40 mM $K^+-induced$ contraction in a dose-dependent manner $(10^{-10}{\sim}10^{-6}\;M)$ in the endothelium-rubbed aortic strips of both strains. However, there was no significant difference in these relaxations between WKY and SHR. 8-bromo-cyclic guanosine monophosphate (8-Br-cGMP), a cell membrane-permeable derivative of cGMP relaxed the 40 mM $K^+-induced$ contraction in a dose-dependent manner $(10^{-6}{\sim}10^{-4}\;M)$ in the endothelium-rubbed aortic strips of both strains. Also norepinephrine $(10^{-6}\;M)-induced$ contractions in normal and Ca-free Tyrode's solution were suppressed by the pretreatment with 8-Br-cGMP $(10^{-4}\;M)$ in either strain. However, the amplitudes of suppression induced by 8-Br-cGMP were greater in SHR than that in WKY. Basal $^{45}Ca$ uptake and 40mM $K^+-stimulated\;^{45}Ca$ uptake were not suppressed by pretreatment with 8-Br-cGMP $(10^{-4}\;M)$ in single aortic smooth muscle cells of both SHR and WKY. From the above results, it is suggested that cGMP decreases Ca sensitivity in vascular smooth muscle cells and that the impaired endothelium-dependent relaxation in the aortic strips of SHR is not the result of a reduced vascular response to EDRF.