• The Korean Journal of Pesticide Science
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• v.13 no.3
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• pp.185-189
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• 2009

A monoterpenoid compound, benzylideneacetone (BZA), is a metabolite of an entomopathogenic bacterium, Xenorhabdus nematophila. Its primary biological activity is an inhibitor of phospholipase $A_2$, which catalyzes the committed step of biosynthesis of various eicosanoids that are critically important to mediate insect immune responses. When BZA was applied to two-spotted spider mite, Tetranychus urticae, it exhibited a dose-dependent mortality in leaf-disc assay. Subsequently BZA was tested against T. urticae infesting apples in a field orchard, in which it showed a significant control efficacy, which was not statistically different with that of a commercial acaricide. BZA also had significant antibacterial activities against three species of plant pathogenic bacteria when it was added to the bacterial cultures, in which it showed the highest inhibitory activity against a bacterial wilt-causing pathogen, Ralstonia solanacearum. The bacterial pathogen caused significant disease symptom to young potato plants. However, BZA significantly suppressed the disease occurrence. This study suggests that BZA can be used to develop a novel crop protectant to control mite and bacterial pathogen.

• Korean Chemical Engineering Research
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• v.53 no.6
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• pp.672-676
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• 2015

Spherical phospholipid bilayers, vesicles, were formed with respect to phase of each layer via a double emulsion technique. The conversion of phosphatidylcholine (PC) to phosphatidic acid (PA) at the outer layer, caused by phospholipase D (PLD), induced a curvature change in the vesicles, which eventually led them to fuse each other. The effect of the lipid layer physical-properties on the PLD-induced vesicle fusion was investigated using the fluorescence intensity change. 8-Aminonaphthalene-1,3,6-trisulfonic acid disodium salt(ANTS) and p-Xylene-bis(N-pyridinium bromide)(DPX) were encapsulated in the vesicles, respectively, for the quantification of the fusion. The fluorescence scale was calibrated with the fluorescence of a 1/1 mixture of ANTS and DPX vesicles in NaCl buffer taken as 100% fluorescence (0% fusion) and the vesicles containing both ANTS and DPX as 0% fluorescence (100% fusion), considering the leakage into the medium studied directly in a separate experiment using vesicles containing both ANTS and DPX. It was observed that the fusion occurred to the liquid-phase of the inner layer only. The fusion behaviors were very similar for both solid and liquid of the outer layer. However, the leakage was faster for the solid-phase outer-layer than the liquid-phase outer-layer. The difference in the leakage seems to be caused by the lipid concentration and the lateral diffusivity in the layer.

• IMMUNE NETWORK
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• v.5 no.4
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• pp.237-246
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• 2005

Background: Little information is available on the identification and characterization of the upstream regulators of the signal transduction cascades for Mycobacterium tuberculosis (M. tbc)-induced ERK 1/2 activation and chemokine expression. We investigated the signaling mechanisms involved in expression of CCL3 /MIP-1 and CCL4/MIP-1 in human primary monocytes infected with M. tbc. Methods: MAP kinase phosphorylation was determined using western blot analysis with specific primary antibodies (ERK 1/2, and phospho-ERK1/2), and the upstream signaling pathways were further investigated using specific inhibitors. Results: An avirulent strain, M. tbc H37Ra, induced greater and more sustained ERK 1/2 phosphorylation, and higher CCL3 and CCL4 production, than did M. tbc H37Rv. Specific inhibitors for mitogen-activated protein kinase (MAPK) kinase (MEK; U0126 and PD98059) significantly inhibited the expression of CCL3 and CCL4 in human monocytes. Mycobactetia-mediated expression of CCL3 and CCL4 was not inhibited by the Ras inhibitor manumycin A or the Raf-1 inhibitor GW 5074. On the other hand, phospholipase C (PLC) inhibitor (U73122) and protein kinase C (PKC)specific inhibitors ($G\ddot{o}6976$ and Ro31-8220) significantly reduced M. tbc-induced activation of ERK 1/2 and chemokine synthesis. Conclusion: These results are the first to demonstrate that the PLC-PKC-MEK-ERK, not the Ras-Raf-MEK-ERK, pathway is the major signaling pathway inducing M. tbc-mediated CCL3 and CCL4 expression in human primary monocytes.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.21
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• pp.9417-9421
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• 2014

Background: Esophageal cancer is one of the most frequently occurring malignancies and the seventh leading cause of cancer-related deaths in the world. The esophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer worldwide. Materials and Methods: Our goal in this study was to detect phospholipase A2 Group IIA (PLA2G2A) and cyclooxygenase-2 (COX-2) immuno-expression in ESCC in a high-risk population in China. Results: Positive expression of PLA2G2A protein was observed in 57.2% (166/290) of the cases, while COX-2 was found in 257 of 290 samples (88.6%), both PLA2G2A and COX-2 being expressed in 153 cases (52.8%), with a significant agreement (Kappa=0.091, p=0.031).Overexpression of PLA2G2A was significantly correlated with the depth of invasion (p=0.001). Co-expression of PLA2G2A and COX-2 not only significantly correlated with the depth of invasion (p=0.004) but also with TNM stage (p=0.04). Conclusions: Our results showed that in patients with ESCC, PLA2G2A overexpression and PLA2G2A co-expression with COX-2 is significantly correlated with advanced stage. The biological role and pathophysiologic regulation of PLA2G2A and COX-2 overexpression in ESCC deserve further investigation.

• Journal of the Korean Chemical Society
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• v.59 no.1
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• pp.22-30
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• 2015

The effect of diphtheria toxin on cell membrane lipids was studied by examining the phospholipase D (PLD) activity and free fatty acids (FFA) release in HepG2 cells. The diphtheria toxin effects on lipid alteration show apparently maximal at pH 5.1, stimulating PLD activity nearly 3.5 fold and enhancing FFA release approximately 5 fold over the control. These results indicate that the membrane is perturbed and its lipid component is rearranged during the diphtheria toxin translocation. Digitonin, a random membrane perturbing detergent, exhibit about four-fold higher perturbation effect over the diphtheria toxin at neutral pH. This observation suggests that the membrane perturbation induced by diphtheria toxin appears to be rather selective. To investigate the cause of the membrane perturbation, Cibacron blue, an inhibitor of membrane pore formation, and hemagglutinin, an influenza virus with fusion peptide, were tested for their effects on diphtheria toxin action. Cibacron blue decreased the diphtheria toxin effect by almost 50%, but the lipid alteration induced by hemagglutinin was similar to the diphtheria toxin effect. These observations imply that the membrane perturbation induced by diphtheria toxin may be caused by a combination of pore formation and insertion of hydrophobic peptide of toxin to the membrane as well. Additionally, we found that the diphtheria toxin increased the HepG2 cells permeability but the cells viability was maintained at high level at the same time. DNA fragmentation which is related to apoptosis was not induced by the toxin. Under these conditions, we could demonstrate that the lipid alteration of HepG2 cells was brought about by diphtheria toxin at acidic pH.

• Preventive Nutrition and Food Science
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• v.5 no.4
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• pp.213-218
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• 2000

The purpose of the study was to investigate the effects of dietary green tea catechin and vitamin E on the phospholipse {TEX}$A_{2}${/TEX} activity and th antioxidative defense system in streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley male rats weighing 100$\pm$10 gm were randomly assigned to one normal and five STZ-induced diabetic groups. The diabetic groups were assigned either a catechin-free diet (DM group), 0.5% catechin diet (DM-0.5C group), 1% catechin diet (DM-1C group), vitamin E-free diet (DM-0E group), and 400 mg vitamin E per kg diet (DM-400E group) according to the levels of dietary catechin or vitamin E supplementation. The vitamin E levels of the normal, DM, DM-0.5C, and DM-1C groups were 40 mg per kg diet. Diabetes was experimentally induced by an intravenous injection of streptozotocin after 4 weeks of feeding the five experimental diets. The animals were sacrificed on the 6th day of he diabetic state. The body weight gains were lower in all five diabetic groups after the STZ injection. The platelet phospholipase {TEX}$A_{2}${/TEX}({TEX}$PLA_{2}${/TEX}) activity in the diabetic groups was higher than that in the normal group. However, the enzyme activity in the DM-0.5C, DM-1C, and DM-400E groups was lower than that in the DM and DM-0E groups. The cytochrome {TEX}$P_{450}${/TEX} and cytochrome {TEX}$b_{5}${/TEX} content and NADPH-cytochrome {TEX}$P_{450}${/TEX} reductase activity were about 50~110% higher in the DM and DM-0E groups than in the normal group, yet significantly reduced by either catechin or vitamin E supplementation. The superoxide dismutase (SOD) content in the liver did not differ significantly in any of the groups. However, the glutathione peroxidase (GSHpx) activity was generally lower in the diabetic groups, compared with the normal group, whereas that of the DM-0.5C, DM-1C, and DM-400E groups was significantly higher compared with that of the DM and DM-0E groups. The levels of thiobarbituric acid reactive substances (TBARS) in the liver tissue were 148% and 201% higher in the DM and DM-0E groups, respectively, compared with the normal group, however, these levels were reduced by either catechin or vitamin E supplementation (DM-0.5, DM-1C and DM-400E). Accordingly, the present results indicate that STZ-induced diabetic rats exhibited an imbalance between free radical generation and scavenger systems in the liver which led to the acceleration of lipid peroxidation. However, these abnormalities were reduced and the antioxidative defense system was restored by either dietary catechin or vitamin E supplementation. In conclusion, the effects of dietary catechin or vitamin E in streptozotocin-induced diabetic rats would appear to inhibit lipid peroxidation as an anti-oxidant by regulating the activity of {TEX}$PLA_{2}${/TEX}.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.12
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• pp.298-305
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• 2019

Cudrania tricuspidata has been reported to have many biological activities, including anti-inflammatory, anti-cancer, and antioxidant properties. However, the effects of C. tricuspidata root extract (CTE) on human platelet aggregation induced by collagen as well as the signaling pathways involved remain unknown. In the present study, we investigated the effect of CTE on human platelets. CTE inhibited platelet aggregation via down-regulation of thromboxane A₂ (TXA₂) by blocking cyclooxygenase-1 (COX-1) activity and intracellular Ca²⁺ mobilization in collagen-induced platelets. CTE also reduced the phosphorylation of phospholipase C (PLC) γ2 and syk. CTE regulated platelet aggregation via cyclic guanosine monophosphate (cGMP)-dependent phosphorylation of vasodilator-stimulated phosphoprotein (VASP) Ser²³⁹. In addition, administration of CTE (50 and 100 mg/kg) significantly reduced hyper-aggregated platelet aggregation by collagen (5 ㎍/mL) without hepatotoxicity in HFD (high fat diet)-fed rats. Taken together, these results suggest that CTE has anti-platelet effects both in vitro and in vivo. Therefore, CTE may be an effective therapeutic and preventive agent for cardiovascular disease, and is a safe and natural product.

• Korean journal of applied entomology
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• v.53 no.3
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• pp.271-280
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• 2014

Some bacterial metabolites of Xenorhabdus nematophila (Xn) inhibit phospholipase $A_2$ ($PLA_2$) activity to shutdown eicosanoid biosynthesis in target insects. However, little has been known about the target insect $PLA_2$ of these bacterial metabolites. Eight bacterial metabolites identified in Xn culture broth exhibited significant insecticidal activities against larvae of both lepidopteran species of Plutella xylostella and Spodoptera exigua. Moreover, these bacterial metabolites significantly enhanced insecticidal activities of Bacillus thuringiensis (Bt). To determine target $PLA_2$, we cloned and over-expressed cellular $PLA_2$ ($SecPLA_2$) of S. exigua. Purified $SecPLA_2$ catalyzed phospholipids derived from the fat body and released several polyunsaturated fatty acids. Most Xn metabolites significantly inhibited $SecPLA_2$ activity, but were different in their inhibitory activities. There was a positive correlation between the inhibition of $SecPLA_2$ and the enhancement of Bt insecticidal activity. These results indicate that $SecPLA_2$ is a molecular target inhibited by Xn metabolite.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.503-516
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• 2001

Background : The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. Method : In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung. Results : In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils. Conclusion : A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.

• Korean Chemical Engineering Research
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• v.49 no.4
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• pp.480-484
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• 2011

In this study, degumming process was carried out for reducing to less than 10 ppm of phosphorus contents and primary properties of crude canola oil including 0.64 mgKOH/g of acid value, 0.09% of water contents, 0.13% of insoluble impurities, and 40 ppm of phosphorus contents. Efficiency of water degumming and enzymatic degumming was compared for the selection of suitable process obtaining feedstock of biodiesel. Degumming method was determined for preparation of raw material of biodiesel, and reaction conditions were also established. The most effective conditions for water degumming were 2% distilled water (w/w oil), $30^{\circ}C$ of reaction temperature, 900 rpm of agitation speed, and 30 min of reaction time, respectively. In case of enzymatic degumming, optimal conditions were found to be 90 ppm of phospholipase A2 (w/w oil), $50^{\circ}C$ of reaction temperature at pH 5, respectively. When comparing water degumming with enzymatic degumming, efficiency of enzymatic degumming was better than water degumming. However, water degumming method was much more suitable for the production of biodiesel feedstock considering reaction time and process feasibility.