• Korean Journal of Plant Resources
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• v.27 no.1
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• pp.22-28
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• 2014

In this study, we conducted the anti-HIV-1 enzymes assay in vitro and its active components were predicted by QSAR in silico for the elucidation of action mechanism on anti-HIV of natural resources. The extracts of Gardenia jasminoides var. radicans Makino were tested for their inhibitory effects on the reverse transcriptase (RT), protease and ${\alpha}$-glucosidase. In the enzyme inhibition assay, the methanol extracts of Gardenia jasminoides var. radicans Makino stem showed a strong activity of 32.5% on the enzyme activity to cleave an oligopeptide, resembling one of the cleavage sites in the viral polyprotein which can only be processed by HIV-1 protease. Moreover the methanol extracts of stem exhibited alpha-glucosidase inhibitory activities of 26.1%. The methanol extracts ($100{\mu}g/ml$) of stem showed a weak activity of 13.4% on anti-HIV-1 RT using Enzyme Linked Oligonucleotide Sorbent Assay (ELOSA) method. However, all extracts of leaf and stem didn't exhibit the HIV-1-induced cytopathic effects with IC (inhibitory concentration) of $100{\mu}g/ml$ in HIV-1-infected human T-cell line. From these results, it is suggested that Gardenia jasminoides var. radicans Makino extracts may possibly be involved in the inhibition of reverse transcriptase, protease and alpha-glucosidase but can't vitally concerned with the viral replication in vitro.

• Food Science and Preservation
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• v.24 no.7
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• pp.1007-1016
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• 2017

Melania snail (Semisulcospira libertina) was traditionally used as the healthy food in Korea. It was generally known to improve liver function and heal a diabetes. The aim of this study was to elucidate the anti-diabetic mechanism of melanian snail hydrolysates treated with protamex (MPH) by investigating the inhibitory action on protein tyrosine phosphatase 1B (PTP1B), the improving effect on the insulin resistance in C2C12 myoblast and the protective effect for pancreatic beta-cell (INS-1) under the glucose toxicity. The melania snail hydrolysates treated with protamex (MPH), which showed the highest degree of hydrolysis (43%), and inhibited effectively PTP1B activity ($IC_{50}=15.42{\pm}1.1{\mu}g/mL$), of which inhibitory effect was higher than usolic acid, positive control ($IC_{50}=16.65{\mu}g/mL$). MPH increased the glucose uptake in C2C12 myoblast treated with palmitic acid. In addition, MPH increased insulin mRNA expression level by over 160% with enhanced cell viability in INS-1 cell under the high glucose concentration (30 mM). These results suggest that MHP may improve the diabetic symptom by the inhibiting the PTP1B activity, increasing the glucose uptake in muscle cell and protecting the pancreatic beta-cell from glucose toxicity.

• Archives of Pharmacal Research
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• v.21 no.6
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• pp.671-676
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• 1998

Five hundred and seventy clinical strains of Pseudomonas aeruginosa were isolated from August 1993 to August 1994 in Korea and screened for their resistance to ciprofloxacin, norfloxacin, and ofloxacin. Among these, two P. aeruginosa strains (PA150 and PA300) were selected based on their strong resistance (MICs > 50mcg/ml) to all three quinolones. The susceptible strain as well as two resistant strains had proton gradient-dependent efflux system. Efflux system in PA300 showed different specificities to ofloxacin and ciprofloxacin while PA150 had less permeability for ofloxacin. Ofloxacin had a less inhibitory action on DNA synthesis in permeabilized cells of PA150 and PA300 than 1771M. When quinolone resistance determining region (QRDR) in gyrA was sequenced, PA300 had one missense mutation, Asn 116Tyr, which was newly reported in this work. The results showed that PA150 became ofloxacin resistant by reduced ofloxacin accumulation due to the existence of efflux system and low permeability, while resistance of PA300 was due to the efflux system and a mutation in QRDR of gyrA -the target site of quinolone.

• BMB Reports
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• v.48 no.5
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• pp.277-282
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• 2015

We demonstrated previously that a disintegrin and metalloproteinase 15 (ADAM15) is released into the extracellular space as an exosomal component, and that ADAM15-rich exosomes have tumor suppressive functions. However, the suppressive mechanism of ADAM15-rich exosomes remains unclear. In this study, we show that the ADAM15 ectodomain is cleaved from released exosomes. This shedding process of the ADAM15 ectodomain was dramatically enhanced in conditioned ovarian cancer cell medium. Proteolytic cleavage was completely blocked by phenylmethylsulfonyl fluoride, indicating that a serine protease is responsible for exosomal ADAM15 shedding. Experimental evidence indicates that the ADAM15 ectodomain itself has comparable functions with those of ADAM15-rich exosomes, which effectively inhibit vitronectininduced cancer cell migration and activation of the MEK/extracellular regulated kinase signaling pathway. We present a tumor suppressive mechanism for ADAM15 exosomes and provide insight into the functional significance of exosomes that generate tumor-inhibitory factors. [BMB Reports 2015; 48(5): 277-282]

• Journal of Microbiology and Biotechnology
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• v.27 no.12
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• pp.2129-2140
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• 2017

Silibinin is the major active component of silymarin, extracted from the medicinal plant Silybum marianum. Silibinin has potent antibacterial activity; however, the exact mechanism underlying its activity has not been elucidated. Here, we investigated the novel mechanism of silibinin against Escherichia coli. Time-kill kinetic assay showed that silibinin possess a bactericidal effect at minimal inhibitory concentration (MIC) and higher concentrations (2-and 4-fold MIC). At the membrane, depolarization and increased intracellular $Ca^{2+}$ levels were observed, considered as characteristics of bacterial apoptosis. Additionally, cells treated with MIC and higher concentrations showed apoptotic features like DNA fragmentation, phosphatidylserine exposure, and caspase-like protein expression. Generally, apoptotic death is closely related with ROS generation; however, silibinin did not induce ROS generation but acted as a scavenger of intracellular ROS. These results indicate that silibinin dose-dependently induces bacterial apoptosis-like death, which was affected by ROS depletion, suggesting that silibinin is a potential candidate for controlling bacteria.

• Korean Journal of Medicinal Crop Science
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• v.16 no.1
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• pp.27-32
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• 2008

This study aimed to investigate the anti-allergic activity and the mechanism of action of Crassirhizomae rhizoma (CR). The extract of CR exhibited potent inhibitory activity in mast cells; its $IC_{50}$ values were $31.2{\pm}1.5{\mu}g/m{\ell}$ for rat basophile leukemia (RBL)-2H3 mast cells and $51.5{\pm}2.1{\mu}g/m{\ell}$ for bone marrow-derived mast cells by antigen stimulation. It also suppressed the expression of TNF-${\alpha}$ and IL-4 mRNAs in RBL-2H3 cells. In an in-vivo animal allergy model, it inhibited a local allergic reaction, passive cutaneous anaphylaxis (PCA), in a dose-dependent manner. With regard to the mechanism of action, CR inhibited the activating phosphorylation of Syk kinase, a key signaling protein for the activation of mast cells. Taken together, these results strongly suggested that the anti-allergic activity of CR is mediated through the inhibition of histamine release and allergic cytokine production by the inhibition of Syk in mast cells.

• Journal of Environmental Science International
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• v.13 no.8
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• pp.711-719
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• 2004

The effect of nickel (Ni) on growth and some tolerance strategies with regard to heavy metal tolerance mechanism was investigated in radish (Raphanus sativus) seedlings. The protective effect of histidine on nickel stress conditions was also monitored. The seedling growth decreased with an increase in metal concentrations. The inhibitory effect was more pronounced in the root elongation than in the shoot elongation. Increasing Ni supply showed a progressive increase of Ni concentrations in the roots and shoots. Ni content was higher in the shoots than in the roots. In the presence of nickel, radish exhibited an antioxidative defense mechanism, as evidenced by the elevated malondialdehyde(MDA), showing that nickel is an efficient inducer of lipid peroxidation. Exposure of radish to elevated concentrations of nickel was accompanied by an increase in the proline content. Supplemental histidine in the presence of Ni ameliorated metal-induced growth inhibition and lipid peroxidation. Combinations of Ni and histidine resulted in a significant decline in proline content compared with Ni stress alone, indicating that histidine may provide protection against the adverse effect of Ni stress. From the results it is suggested that histidine is an efficient chelator by complexing metal ion within the plant and may playa role in nickel tolerance implicated in metal detoxification.

• IMMUNE NETWORK
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• v.12 no.6
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• pp.240-246
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• 2012

Natural killer (NK) cells play a pivotal role in early surveillance against virus infection and cellular transformation, and are also implicated in the control of inflammatory response through their effector functions of direct lysis of target cells and cytokine secretion. NK cell activation toward target cell is determined by the net balance of signals transmitted from diverse activating and inhibitory receptors. A distinct feature of NK cell activation is that stimulation of resting NK cells with single activating receptor on its own cannot mount natural cytotoxicity. Instead, specific pairs of co-activation receptors are required to unleash NK cell activation via synergy- dependent mechanism. Because each co-activation receptor uses distinct signaling modules, NK cell synergy relies on the integration of such disparate signals. This explains why the study of the mechanism underlying NK cell synergy is important and necessary. Recent studies revealed that NK cell synergy depends on the integration of complementary signals converged at a critical checkpoint element but not on simple amplification of the individual signaling to overcome intrinsic activation threshold. This review focuses on the signaling events during NK cells activation and recent advances in the study of NK cell synergy.

• YAKHAK HOEJI
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• v.37 no.3
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• pp.270-277
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• 1993

It is well known that lipidperoxide, formed in vivo, induced the denaturation of enzyme and destruction of cell membrane to acute injury of tissue. Aralia elata have physiological activates, the improvement of lipid metabolism, antidiabetic activity etc., which was thought to have the relationship to lipid peroxidation. The anti-lipidperoxidative effect of Aralia elata have not yet established. In this study, we examined the anti-lipidperoxidative effects of Aralia elata (Butanol fraction) on CCI$_{4}$ induced lipidperoxidation in rats, and elucidated the anti-lipidperoxidative mechanism. In rat liver homogenate intoxicated with CCI$_{4}$ (0.5 ml/100g), BuOH fraction of Aralia elata (80 mg/Kg/day) exhibited 85.41% anti-lipidperoxidative effect but in serum 69.63% inhibitory effects, respectively. In mitochondrial and microsomal fraction showed inhibition of 55.85% and 69.30%, respectively. In order to elucidate the mechanism of anti-lipidperoxidation effects of Aralia elata, enzymatic (NADPH dependent) and non-enzymatic (Ascorbic acid catalyzed) reaction, in vitro, were performed. In enzymatic reation, Aralia elata exhibited 59.43% anti-lipidperoxidation effects, but in non-enzymatic reaction exhibited 43.27% inhibition. Therefore, it is noteworthy that antioxidative power of them may mainly results from the inhibition by enzymatic reaction.

• The Journal of Korean Obstetrics and Gynecology
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• v.21 no.2
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• pp.152-165
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• 2008

Purpose: It is the purpose of this study to investigate the anti-inflammatory effects and mechanism of cheukbaekjurpihwan(CBJPH) extract on LPS (lipopolysaccharide)-induced inflammatory mediators in murine peritoneal macrophages. Methods: To evaluate anti-inflammatory effects of CBJPH extract, the production of cytokines(TNF-${\alpha}$(tumor necrosis factor-alpha), IL(interleukin)-6, IL-12) and NO(nitric oxide) was measured in vitro and in vivo. And western blot analysis has been done to look into the mechanism. Results: CBJPH extract reduced LPS-induced NO, TNF-${\alpha}$ and IL-6, IL-12 productions in peritoneal macrophages. CBJPH extract inhibited the activation of JNK(c-Jun N-terminal kinase), but didn't inhibit the activation of MAPKs (mitogen-activated protein kinases) such as p38, ERK1/2(extracelluar signal-regulated kinase1/2) and the degradation of $I_{\kappa}B-{\alpha}$(inhibitory kappa B-alpha) in the LPS-stimulated peritoneal macrophages. CBJPH extract suppressed LPS-induced endotoxin shock and the productions of TNF-${\alpha}$, but not of IL-6, after an oral administration of CBJPH extract Conclusion: CBJPH extract suppressed the productions of LPS-induced NO and cytokines by preventing JNK from phosphorylation, which may provide a clinical basis for anti-inflammatory properties of CBJPH.