• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.127-138
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• 1996

The effects of adenosine analogues on the electrically-evoked acetylcholine(ACh) release and the influence of ischemia on the effects were studied in the rat hippocampus. Slices from the rat hippocampus were equilibrated with $0.1{\mu}M$ $[^3H]-choline$ and the release of the labelled product, $[^3H]-ACh$, was evoked by electrical stimulation(3 Hz, 2 ms, 5 $VCm^{-1}$ and rectangular pulses for 2 min), and the influence of various agents on the evoked tritiumoutflow was investigated. Ischemia(10 min with 95% $N_2$ + 5% $CO_2$) increased both the basal and evoked ACh release. These increases were abolished by glucose addition into the superfused medium, and they significantly inhibited either by 0.1 & $0.3{\mu}M$ TTX pretreatment or by removing $Ca^{++}$ in the medium. MK-801($1{\sim}10{\mu}M$), a specific NMDA receptor antagonist, and glibenclamide $(1{\mu}M)$, a $K^+-channel$ inhibitor, did not alter the evoked ACh release and nor did they affect the ischemia-induced increases In ACh release. However, polymyxin B(0.03 mg), a specific protein kinase C inhibitor, significantly inhibited the effects of ischemia on the evoked ACh release. Adenosine and $N^6-cyclopentyladenosine$ decreased the ACh release in a dose dependent manner in ischemic condition, though the magnitude of inhibition was far less than those in normal(normoxic) condition. However, the treatment with $5{\mu}M$ DPCPX, a potent $A_1-adenosine$ receptor antagonist, potentiated the ischemia-effect. These results indicate that the evoked-ACh release is potentiated by ischemia, and this process being most probably mediated by protein kinase C, and that the decreased effect of ACh release mediated by $A_1-adenosine$ receptor is significantly inhibited in ischemic state.

• Journal of Life Science
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• v.25 no.5
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• pp.607-614
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• 2015

Cancers are the largest cause of mortality and morbidity all over the world. Cordycepin, an adenosine analog, is a major functional component of the Cordyceps species, which has been widely used in traditional Oriental medicine. Over the last decade, this compound has been reported to possess many pharmacological properties, such as an ability to enhance immune function, as well as anti-inflammatory, antioxidant and anti-cancer effects. Recently, numerous studies have reported interesting properties of cordycepin as a chemopreventive agent as well. There is an accumulating body of experimental evidences suggesting that cordycepin impedes cancer progression by promoting apoptosis, inducing cell cycle arrest, modulating intracellular signaling pathways, and inhibiting invasion and metastasis of cancer cells. In many cancer cell lines, cordycepin inhibits growth and cell cycle progression by inducing arrest of the G2/M phase, resulting from the inhibition of retinoblastoma protein phosphorylation and induction of cyclin-dependent kinase inhibitors. To induce apoptosis, cordycepin activates the extrinsic and intrinsic pathways, which promotes reactive oxygen species generation and the downstream activation of kinase cascades. Cordycepin also can activate alternative pathways to cell death such autophagy. In addition, cordycepin can inhibit the pro-metastatic processes of cancer cell detachment, migration, and invasion through a variety of mechanisms, including the nuclear factor-kappa B and activated protein-1 signaling pathways. In this review, we summarized the variety of action mechanisms by which cordycepin may mediate chemopreventive effects on cancer and discussed the potential of this natural product as a promising therapeutic inhibitor of cancer development.

• Microbiology and Biotechnology Letters
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• v.26 no.3
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• pp.244-249
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• 1998

An extracellular polysaccharide, methylan, was produced under the specific conditions by Methylobacterium organophilum from methanol. The specific growth rate of cells was approximately constant regardless of C/N ratio and the specific product yield was maximum at a C/N ratio of 30. Methylan production was suppressed by the deficiency of mineral ions such as Mn$^{++}$ or Fe$^{++}$ ion. The optimal pH for cell growth and methylan production was 7. Whereas the optimal temperature for cell growth was found to be 37$^{\circ}C$, that for methylan production was 3$0^{\circ}C$. The methanol concentration above 4% completely inhibited the cell growth. The initial methanol concentration for the maximal production of methylan was 0.5% (v/v) and above this concentration, methylan production was markedly inhibited. To overcome the substrate toxicity and inhibition for both cell growth and methylan production, a fed-bach culture of intermittent feeding within 5 g/l methanol was conducted under the optimal culture condition. Methylan production of was stimulated by nitrogen limitation and methylan was accumulated up to 8.7 g/1 and cell mass also increased up to 12.4 g/l.

• Journal of Microbiology and Biotechnology
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• v.30 no.11
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• pp.1659-1669
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• 2020

1,3-α-3,6-anhydro-L-galactosidase (α-neoagarooligosaccharide hydrolase) catalyzes the last step of agar degradation by hydrolyzing neoagarobiose into monomers, D-galactose, and 3,6-anhydro-L-galactose, which is important for the bioindustrial application of algal biomass. Ahg943, from the agarolytic marine bacterium Gayadomonas joobiniege G7, is composed of 423 amino acids (47.96 kDa), including a 22-amino acid signal peptide. It was found to have 67% identity with the α-neoagarooligosaccharide hydrolase ZgAhgA, from Zobellia galactanivorans, but low identity (< 40%) with the other α-neoagarooligosaccharide hydrolases reported. The recombinant Ahg943 (rAhg943, 47.89 kDa), purified from Escherichia coli, was estimated to be a monomer upon gel filtration chromatography, making it quite distinct from other α-neoagarooligosaccharide hydrolases. The rAhg943 hydrolyzed neoagarobiose, neoagarotetraose, and neoagarohexaose into D-galactose, neoagarotriose, and neoagaropentaose, respectively, with a common product, 3,6-anhydro-L-galactose, indicating that it is an exo-acting α-neoagarooligosaccharide hydrolase that releases 3,6-anhydro-L-galactose by hydrolyzing α-1,3 glycosidic bonds from the nonreducing ends of neoagarooligosaccharides. The optimum pH and temperature of Ahg943 activity were 6.0 and 20℃, respectively. In particular, rAhg943 could maintain enzyme activity at 10℃ (71% of the maximum). Complete inhibition of rAhg943 activity by 0.5 mM EDTA was restored and even, remarkably, enhanced by Ca²⁺ ions. rAhg943 activity was at maximum at 0.5 M NaCl and maintained above 73% of the maximum at 3M NaCl. K_m and V_max of rAhg943 toward neoagarobiose were 9.7 mg/ml and 250 μM/min (3 U/mg), respectively. Therefore, Ahg943 is a unique α-neoagarooligosaccharide hydrolase that has cold- and high-salt-adapted features, and possibly exists as a monomer.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.10
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• pp.1241-1247
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• 2007

Contents of polyphenol compounds and the physiological activity of extracts from Grifola frondosa by water and methanol extraction were investigated to determine their functional effects. A functional beverage was developed using the extracts. The yield and phenolic compounds content of the water extracts were highest (49.2% and 327 mg/100 g, respectively), while for the methanol extraction method they were 28.7% and 130 mg/100 g, respectively. DPPH (1,1-diphenyl-2-picrylhydrazyl) radical scavenging activity was 76.3% for the water extract and 65.4% for methanol extract, whereas the superoxide dismutase (SOD)-like activity was low ($26.3{\sim}36.8%\;at\;1,000{\mu}g/mL$ concentration) Angiotensin converting enzyme (ACE) inhibitory effect of water extract (75.1%) was higher compared to the methanol extracts (41.2%). Tyrosinase inhibition activity was 42.5% for the water extracts and 31.8% for the methanol extracts at $1,000{\mu}g/mL$ concentration. The most acceptable formulation for G. frondosa beverage developed was 0.5% G. frondosa water extract, 8.0% oligosaccharide, 2.0% green tea extract, 2.0% jujube extract, 1.0% Solomon's seal extract, 0.01% vitamin C, and 2.0% apple extract. The final product had 9.8 Brix and color values of L, 35.2+1.1; a, 3.2+0.2; b, 13.6+0.3.

• Journal of the East Asian Society of Dietary Life
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• v.22 no.6
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• pp.812-817
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• 2012

This study was performed to investigate the antioxidant activities and the melanin inhibitory effects of Hippophae rhamnoides L. fruit extracts. Two in vitro methods were used; the 1,1-diphenyl-2-picrylhydrazyl (DPPH) method to determine antioxidant activity and measurements of the inhibitory effects of tyrosinase activity to determine melanogenesis in B16/F10 melanoma cells. The radical scavenging activity of the extract was 56.0% at $700{\mu}g/mL$, similar to ascorbic acid (56.9%), in the DPPH assay. The tyrosinase inhibitory activity of the extract was 52.1% and 73.4% at 100 and $500{\mu}g/mL$, which is also similar to ascorbic acid. In B16/F10 mouse melanoma cells, the extract inhibited melanin synthesis by 56% at $500{\mu}g/mL$, a more prominent inhibition of melanin synthesis compared to extracts from arbutin. These results suggest that extracts from H. rhamnoides L. have antioxidant activity and skin-whitening effects; allowing their application in cosmetics as a natural product.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.6
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• pp.1041-1046
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• 2001

Solutions of fructose, glucose and sucrose were heated without catalyst at various temperature for different length of time. Changes in the formation of early caramelization product and browning intensity as well as pH of heated sugar solutions were determined. Reducing powers of caramelization products (CP) and their inhibitory effects on polyphenol oxidase (PPO) were also determined and their correlations were discussed. The early CP and browning intensity increased with temperature and time, in the order of heated fructose>sucrose>glucose solutions (p<0.005), while pH decreased. pHs of sugar solutions heated at 20$0^{\circ}C$ showed in the range of 3.32 ~ 3.50. Reducing power of CP as well as their inhibitory effect on PPO also increased with temperature and time, respectively. Among sugar solutions, reducing power showed the same trends as above at both 15$0^{\circ}C$ and 17$0^{\circ}C$ (p<0.001). However, those of heated fructose solutions were the highest in the early stage, while those of heated sucrose solutions were the highest in the final stage at 20$0^{\circ}C$. This is due to the difference in CP formed. Sucrose solution heated at 20$0^{\circ}C$ showed the highest inhibitory effect, reducing PPO activity by 34.6%. From these results, it is considered that the inhibitory effect of CP on PPO is partly related to their reducing power.

• BMB Reports
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• v.37 no.2
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• pp.185-191
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• 2004

Tissue transglutaminase (tTGase) regulates various biological processes, including extracellular matrix organization, cellular differentiation, and apoptosis. Here we report the protective role of tTGase in the cell death that is induced by the tumor necrosis factor $\alpha$ (TNF-$\alpha$) and ceramide, a product of the TNF-$\alpha$ signaling pathway, in human neuroblastoma SH-SY5Y cells. Treatment with retinoic acid (RA) induced the differentiation of the neuroblastoma cells with the formation of extended neurites. Immunostaining and Western blot analysis showed the tTGase expression by RA treatment. TNF-$\alpha$ or $C_2$ ceramide, a cell permeable ceramide analog, induced cell death in normal cells, but cell death was largely inhibited by the RA treatment. The inhibition of tTGase by the tTGase inhibitors, monodansylcadaverine and cystamine, eliminated the protective role of RA-treatment in the cell death that is caused by TNF-$\alpha$ or $C_2$-ceramide. In addition, the co-treatment of TNF-$\alpha$ and cycloheximide ecreased the protein level of tTGase and cell viability in the RA-treated cells, supporting the role of tTGase in the protection of cell death. DNA fragmentation was also induced by the co-treatment of TNF-$\alpha$ and cycloheximide. These results suggest that tTGase expressed by RA treatment plays an important role in the protection of cell death caused by TNF-$\alpha$ and ceramide.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.11
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• pp.1414-1418
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• 2017

Inhibition of advanced glycation end product (AGE) formation is a valuable therapeutic strategy for the regulation of diabetic complications. This study was conducted to identify potential therapeutic targets of anti-diabetic complications from irradiated mangiferin using AGE formation assay. Radiolytic degradation of the xanthone glucoside mangiferin by gamma-irradiation resulted in three degraded mangiferin analogues: mangiferdiol (1), mangiferinol (2), and isomangiferinol (3). Structures of the three newly generated compounds were characterized by interpretation of nuclear magnetic resonance ($^1H$, $^{13}C$ NMR, $^1H-^1H$ COSY, HSQC, HMBC, and NOESY) and mass spectroscopic data. The anti-diabetic complication of the generated mangiferin derivatives were tested using in vitro AGE formation method. Among the tested degraded products, mangiferinol (2) and isomangiferinol (3) exhibited significantly improved potency against AGE formation inhibitory activities with $IC_{50}$ values of $5.6{\pm}0.8$ and $7.6{\pm}0.9{\mu}M$, respectively. This result implies that xanthone derivatives generated from gamma-irradiated mangiferin might be beneficial for prevention of diabetic complication and related diseases.

• Journal of Soil and Groundwater Environment
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• v.9 no.3
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• pp.49-55
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• 2004

A soil enrichment LYF-1 culture from a contaminated site, which could reductively dechlorinate 900 $\mu$M (ca. 150 mg/L) of tetrachloroethylene (PCE) stoichimetrically into cis-1,2-dichloroethylene (cis-DCE), was established and characterized. The enrichment culture can use yeast extract, peptone, formate, acetate, lactate, pyruvate, citrate, succinate, glucose, sucrose, and ethanol as electron donors for dechlorination of PCE. Addition of NO$_2$$^{[-10]}$ and NO$_3$$^{[-10]}$ as alternative electron acceptors showed complete inhibition of PCE dechlorination, but S$_2$O$_3$$^{-2}$ , SO$_3$$^{-2}$ and SO$_4$$^{-2}$ had no significant effect on PCE dechlorination. The enrichment culture was attached to ceramic media in an anaerobic fixed-bed reactor. The fixed-bed reactor showed more than 99％ of PCE degradation in the range of PCE loading rate of 0.13-0.78 $\mu$moles/L/hr. The major end product of PCE dechlorination was cis-DCE.