• Preventive Nutrition and Food Science
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• v.22 no.3
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• pp.203-210
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• 2017

The antioxidant and antimicrobial activities of three kinds of strawberry ethanol extracts from Robus corchorifolius L. f. (RCL), Rubus parvifolius L. var. parvifolius (RPL), and Duchesnea chrysantha Miq. (DCM) were investigated. The RPL was highest (P<0.05) in phenolic, flavonoid, and anthocyanin contents. 2,2-Diphenyl-1-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) radical scavenging activities of RPL and DCM extracts were higher than that of RCL (P<0.05). Hydrogen peroxide scavenging activity of RPL was high compared to DCM and RCL (P<0.05). RCL exhibited a significant (P<0.05) potent antioxidant activity in nitric oxide radical inhibition. Inhibition diameter zone (nearest mm) of extracts against the test bacteria ranged from 11.5 in RCL to 12.5 in DCM against Staphylococcus aureus, from 10.5 in RCL to 13.5 in DCM against Streptococcus pneumoniae, from 8.5 in DCM to 10.5 in RCL against Escherichia coli, and the same inhibition of 10 mm in three of the extracts against Klebsiella pneumoniae. However, there was no inhibition against fungi Aspergillus niger and Candida albicans. Three of the extracts had the same minimum inhibitory concentration values of 12.50, 12.50, and $6.25{\mu}g/mL$ against S. aureus, K. pneumoniae, and S. pneumoniae, respectively. On the other hand, MIC values of 12.50, 12.50, and $6.50{\mu}g/mL$ were recorded for RPL, DCM, and RCL against E. coli, respectively. The result of present study revealed that extracts from three kinds of strawberries could be potential candidates as antioxidant and antimicrobial sources for functional food industries.

• Biomolecules & Therapeutics
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• v.21 no.6
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• pp.447-453
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• 2013

Chondroitin sulfate proteoglycan (CSPG) inhibits neurite outgrowth of various neuronal cell types, and CSPG-associated inhibition of neurite outgrowth is mediated by the Rho/ROCK pathway. Mesenchymal stromal/stem cells (MSCs) have the potential to differentiate into neuron-like cells under specific conditions and have been shown to differentiate into neuron-like cells by co-treatment with the ROCK inhibitor Y27632 and the hypoxia condition mimicking agent $CoCl_2$. In this study, we addressed the hypothesis that a ROCK inhibitor might be beneficial to regenerate neurons during stem cell therapy by preventing transplanted MSCs from inhibition by CSPG in damaged tissues. Indeed, dose-dependent inhibition by CSPG pretreatment was observed during morphological changes of Wharton's jelly-derived MSCs (WJ-MSCs) induced by Y27632 alone. The formation of neurite-like structures was significantly inhibited when WJ-MSCs were pre-treated with CSPG before induction under Y27632 plus $CoCl_2$ conditions, and pretreatment with a protein kinase C inhibitor reversed such inhibition. However, CSPG treatment resulted in no significant inhibition of the WJ-MSC morphological changes into neuron-like cells after initiating induction by Y27632 plus $CoCl_2$. No marked changes were detected in expression levels of neuronal markers induced by Y27632 plus $CoCl_2$ upon CSPG treatment. CSPG also blocked the morphological changes of human bone marrow-derived MSCs into neuron-like cells under other neuronal induction condition without the ROCK inhibitor, and Y27632 pre-treatment blocked the inhibitory effect of CSPG. These results suggest that a ROCK inhibitor can be efficiently used in stem cell therapy for neuronal induction by avoiding hindrance from CSPG.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.1
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• pp.25-30
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• 2006

Lysophosphatidylcholine (LPC), which accumulates in atherosclerotic arteries, has been reported to inhibit endothelium-dependent relaxation (EDR) in many different species. However, the underlying mechanism of LPC-induced inhibition of EDR is still uncertain. In the present study, we measured simultaneously both isometric tension and cytosolic free $Ca^{2+}$ ($[Ca^{2+}]_i$) in rabbit carotid strips, and examined the effect of LPC on tension and $[Ca^{2+}]_i$. In carotid strips with intact-endothelium, high $K^+$ (70 mM) increased both tension and $[Ca^{2+}]_i$, and cumulative addition of acetylcholine (ACh) from 0.1 to $10{\mu}M$ induced dose dependent increase of $[Ca^{2+}]_i$ with concomitant relaxation. In the presence of L-NAME (0.1 mM), ACh increased $[Ca^{2+}]_i$ without affecting the amplitude of high $K^+-induced$ tension. These ACh-induced change of $[Ca^{2+}]_i$ and tension was abolished by removal of endothelium or 10 nM 4-DAMP (muscarinic receptor antagonist) pretreatment. Pretreatment of LPC ($10{\mu}M$) inhibited ACh ($10{\mu}M$)-induced change of tension and $[Ca^{2+}]_i$ in endothelium-intact carotid artery. On the other hand, LPC had no effect on ACh-induced change of tension and $[Ca^{2+}]_i$ in endothelium denuded artery. In $Ca^{2+}$-free external solution, ACh transiently increased $[Ca^{2+}]_i$, and pretreatment of LPC significantly inhibited ACh-induced transient $[Ca^{2+}]_i$ change. Based on the above results, it may be concluded that LPC inhibits the ACh-induced $[Ca^{2+}]_i$ change through inhibition of $Ca^{2+}$ mobilization in vascular endothelial cells, resulting in decreased production of NO and concomitant inhibition of endotheliumdependent vascular relaxation.

• Corrosion Science and Technology
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• v.14 no.2
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• pp.85-92
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• 2015

An on-line corrosion rate measurement system was developed using a personal computer, a data acquisition board and program, and a 2-electrode corrosion probe. Reliability of the developed system was confirmed with through comparison test. With this system, the effect of sodium nitrite ($NaNO_2$) as a corrosion inhibitor were studied on iron and aluminum brass that were immersed in sodium chloride (NaCl) solution. Corrosion rate was measured based on the linear polarization resistance method. The corrosion rates of aluminum brass and iron in 1% NaCl solutions were measured to be 0.290 mm per year (mmpy) and 0.2134 mmpy, respectively. With the addition of 200 ppm of $NO{_2}^-$, the corrosion rates decreased to 0.0470 mmpy and 0.0254 mmpy. The addition of $NO{_2}^-$ caused a decrease in corrosion rates of both aluminum brass and iron, yet the $NO{_2}^-$ acted as a more effective corrosion inhibitor for iron. than aluminum brass.

• Korean Journal of Microbiology
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• v.24 no.2
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• pp.113-118
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• 1986

Optimum temperature and pH of glutamine synthetase activity (E.C. 3.6.1.2.) of R. sphaeroides D-230 was $35^{\circ}C$ and 6.8, respectively. The adenylated state of GS in R. sphaeroides D-230 was stabilized by addition of 0.2mg/ml of cethyltrimethylammoniumbromide. Valine, histidine, proline, isoleucine, and lysine were good nitrogen source for the growth of R. sphaeroides D-230. The growth of R. sphaeroides D-230 in $N_2,\;NaNO_3\;or\;NH_4Cl$ as sole nitrogen source was lower than in any otherculture conditions. GS activity was inhibited, more or less, by various amino acid. THe relative inhibition rate of the enzyme by added 7mM arginine, $NH_4Cl,\;N_2,\;and\;NaNO_3$ was 63.8%, 26.79%, 6.24%, and 10.64%, drespectively. THe hydrogen evolution of R. sphaeroides D-230 grown in N-limited media was inhibited by 0.1mM MSX, irreversible GS inhibitor. GS activity was completely inhibited by 1.0mM MSX but ammonia released maximally at the same concentration of MSX. Ammonia release by added MSX was increased up to 1.0mM MS, but decreased above 1.0mM MSX. It is probably due to inhibition of nitrogenase actixity by MSX. Nitrogenase activity was not inhibited at low concentration of MSX. These results suggests that the inhibition of nitrogenase activity by ammonia is mediated by products of ammonia assimilation rather than by ammonia itself.

• Korean journal of applied entomology
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• v.5_6
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• pp.65-69
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• 1968

The effect of respiratory inhibition was investigated by treating conidia or mycelium of Cochliobolus miyabeanus with phenylmercuric 8-oxyquinolinate (PMQ) or. phenylmercuric acetate (PMA) in terms of $O_2$ up take ul/mg dry weight of cells. The results obtained are as follows: 1. In inhibition of mycelial growth, PMQ gave somewhat less effective than PMA, hut there was no remarkable difference between them, and the two indicated strong inhibitory effect on mycelial growth at the range from 0.01 to 1.0 ppm. 2. In inhibition of conidial respiration, PMA gave somewhat stronger than PMQ except at 0.1ppm, but there was no notable difference between them, and it seemed that there was no inhibitory effect at 0.01ppm. 3. PMQ was stronger than PMA in inhibition of mycelial respiration as compared with the cibudail respiration, ration, and the difference between them was about $10\%$. 4. According to the above results, the inhibitory effect of spore germimation by PMQ was the same as to PMA or somewhat lower than that of PMA. The inhibitiry effect of PMQ on mycelial growth was lower than that of PMA.

• Journal of the Korean Applied Science and Technology
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• v.36 no.1
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• pp.13-22
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• 2019

The aim of the present investigation was to assess the oxidation inhibition by nitrogen oxide scavenging activity and physiological activities. Bioactive compound of proanthocyanidin $69.000{\pm}2.737mg$ catechin equivalents (CE)/g dry weight. Antioxidant effects (nitric oxide radical scavenging activity, nitrite scavenging activity, ${\beta}$-carotene bleaching assay and lipid peroxidation inhibition activity) of distilled water (DW), 70% ethanol and n-butanol extract of turmeric (Curcuma longa L.). Turmeric extracts yield were DW 17.11%, 70% ethanol 15.26% and n-butanol 4.12%, respectively. Oxidation inhibition activity of the samples exhibited a dose-dependent increase. However, in the current study, none of the samples evaluated showed activity as strong as the BHA and trolox. Total flavonoid content was the highest in the n-butanol extract, followed by 70% ethanol and DW extract. Further, nitrite scavenging activity was the highest for the n-butanol extract. As a result of this experiment, the turmeric can be utilized as a valuable and potential natural oxidation inhibition for the functional food industry.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.29-36
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• 1988

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor rsponses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into a ear vein, and then same procedures were performed 1~2 min after treatment with intravenous verapamil. The results are summarized as follows: 1. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylphrine($30{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 3. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$), phenylephrine($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. 4. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$) and phenylephrine($10{\mu}g/kg$) were inhibited by pretreatment with intravenous verapairlil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 5. Pressor responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine($30{\mu}g/kg$) and clonidine($100{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in pithed rats. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that verapamil significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors and the inhibition is greater in alpha-2 adrenoceptor-induced response than in alpha-1 adrenoceptor-induced one, and calcium channel takes part in the process of the pressor response mediated by alpha-1 adrenoceptors as well as alpha-2 adrenoceptors.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.145-153
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• 1991

Human neutrophil cathepsin-G, which has been known as one of the active enzymes causing inflammatory diseases, was purified by two steps procedure involving one size exclusion (Ultorogel AcA54) and one ion exchange (CM-Sephadex) chromatography. Purified HNCGs were cross-reacted with Anti-HNCathepsin-G antibodies which were radised in rabbits and purified by cathepsin-G labeled Sepharose 4B affinity chromatography. HNCGs were effectively inhibited by NSAIDs including phenylbutazone, sulindac, oxyphenbutazone, salicylic acid and salicyluric acid. $IC_{50}_s$ of these drugs for inhibition of Cathepsin G were 0.3-0.8 mM. Other NSAIDs including aspirin showed little or no inhibition effect on the activity of Cathepsin G. These results strongly indicated that NSAIDs which showed inhibition effect on the activity of HNCGs possibly be at least a part of mechanism of action which might be related to direct inhibition of cathepsin G at the tissue destruction sites beside of their known mechanism of action as an anticyclo-oxygenase in treatment of inflammatory diseases. Lipid soluble component of Korean Red Ginseng which was known as an anti-inflammatory agent inhibited HNCGs strongly, but no other fractions did inhibited HNCGs. Antibiotics including novobiosin and rifamycin showed some inhibition effect on HNCGs, i. e.., $IC_{50}$ of these drugs were 2.6 mM and 1.5 mM respectively, and other antibiotics including penicillin G showed no or negligible inhibition effect on the activity of HNCGs. However. tetracyclines inhibited HNCGs very effectively at the concentration of therapeutic range. The inhibition effect of the activity of HNCGs by tetracycline are not related to the N-dimethyl radical on the 4 position of the tetracycline molecule. Furthermore, N-dedimethylated tetracyclines may have beneficial effect for long term treatment of chronic inflammatory diseases without developing any drug resistance to microorganisms.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.3
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• pp.785-791
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• 2005

Corydalis Tuber has traditionally been used for the treatment of water retention in the body. Administration of the aqueous extract of Corydalis Tuber has been known to be effective for the control of pain and treatment of arthritis. It was reported that Corydalis Tuber possesses anti-inflammatory activity and modulates the intestinal immune system. The effect of Corydalis Tuber against LPS-stimulated expressions of COX-2, iNOS, and $IL-1{\beta}$ in cells of the murine RAW 264.7 macrophages was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, reverse transcription-polymerase chain reaction (RT-PCR), $PGE_2$ immunoassay, and NO detection. The aqueous extract of Corydalis Tuber was shown to suppress $PGE_2$ production by inhibition on the LPS-stimulated enhancement of COX-2 enzyme activity, $IL-1{\beta}$, and iNOS expression in the RAW 264.7 macrophages. Present results suggest that Corydalis Tuber exerts anti-inflammatory and analgesic effects probably by suppressing of COX-2, iNOS, and $IL-1{\beta}$ expressions, resulting in inhibition of $PGE_2$ synthesis. Corydalis Tuber has anti-inflammatory and analgesic effects probably by suppressing of COX-2, iNOS, and $IL-1{\beta}$ mRNA expressions, resulting in inhibition of $PGE_2$ and NO synthesis.