• YAKHAK HOEJI
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• v.39 no.1
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• pp.10-13
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• 1995

As a continuation of the previous studies, a third group of thirty five hot aqueous extracts from natural products were screened for platelet activating factor(PAF) receptor binding antagonistic acitivities using rabbit platelet. The results demonstrate that Arctium lappa is potential source of PAF antagonist.

• Culinary science and hospitality research
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• v.13 no.3
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• pp.187-198
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• 2007

Some problems are presented that Korean restaurants in jeonju area don't keep ancient fame, taste and tradition. Therefore, this thesis intends to positively analyse the evaluation of Korean restaurants' menu quality to activate Han brand, centering on Jeonju area. The findings of the study are as follows: First, this thesis named the items of analysis menu quality factor, menu quality evaluation factor, Han brand activating factor. Second, it analysed confirmative factor of menu quality evaluation and found that conformity was $x^2=67.143$, df=14, GFI=0.968, AGFI=0.917, RMR=0.056, NFI=0.902, CFI=0.962. It means that the measure of item variables was selected appropriately. Third, it constructed a menu quality evaluation model of Korean restaurants in Jeonju area and verified hypotheses, such as menu quality factors and their influences on menu quality evaluation, menu quality evaluation factors and their influences on activating of Han brand, and menu quality factors and their influences on activating Han brand. It verified the relations, and, as a result, found them to be positive(+) and selected all of the hypotheses.

• Fisheries and Aquatic Sciences
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• v.5 no.4
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• pp.258-262
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• 2002

Effects of Escherichia coli genomic DNA on the production of phagocyte activating supernatants by the head kidney leucocytes isolated from olive flounder (Paralichthys olivaceus) were investigated. Phagocyte activating activity of the supernatants was estimated by. measuring reactive oxygen species (ROS) production in target head kidney phagocytes. All supernatants from olive flounder head kidney leucocytes-stimulated with E. coli DNA induced significantly (P<0.01) higher ROS production from target pagocytes than the unstimulated control supernatant. Maximum enhancement of chemiluminescent response was observed $5.0-10.0{\mu}g\;mL^{-1}$ of bacterial DNA while the increment ability was decreased significantly (P<0.01) at the concentration of $20.0{\mu}mL^{-1}$. The results demonstrate that olive flounder head-kidney leucocytes stimulated with bacterial DNA release a soluble phagocyte activating cytokines capable of enhancing the respiratory burst activity from target phagocytes.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.1-8
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• 1993

To elucidate involvement of platelet-activating factor (PAF) in cerebral ischemia-reperfusion injury, male Sprague-Dawley rats and albino mice of either sex were subjected to a 10-min bilateral carotid artery occlusion and 6-hr recirculation. The McGraw stroke index in mice was markedly inhibited by PAF antagonists, BN 52021 and CV 6209 (1 mg/kg, i.p., each) When they were administered 10 min before bilateral carotid artery occlusion or 1 hr after reperfusion. The increases in brain water content were significantly attenuated by treatment with BN 52021 or CV 6209 in both animals. BN 52021 exhibited a significant improvement in the postischemic blood pressure change in association with a beneficial effect on the delayed dilatation of pial arterioles after 10 min of ischemia. Thus it is suggested that PAF plays an important role as an endogenous mediator in development of cerebral ischemia-reperfusion injury, and further, specific antagonists to PAF will be able to prevent or reverse the pathological sequelae of cerebral ischemia.

• Archives of Pharmacal Research
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• v.26 no.7
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• pp.554-558
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• 2003

Platelet activating factor acetylhydrolase (PAF-AH) activity has been identified in cerebrospinal fluid (CSF) samples taken from children with meningitis. We reported that PAF-AH activity is significantly increased, by about 3 fold, in patients with meningitis compared to control subjects. Because of limited knowledge about this enzyme in CSF, we examined the biochemical properties of CSF PAF-AH. PAF-AH of CSF was calcium independent, showed a broad pH spectrum and was relatively heat stable. In addition, this enzyme activity was strongly inhibited by phenylmethanesulfonyl fluoride (PMSF), partially inhibited by p-bromophenacylbromide (p-BPB), uninhibited by iodoacetamide, and moderately stimulated by dithiothreitol (DTT). PAF-AH of CSF did not degrade phospholipid with a long chain fatty acyl group at sn-2 position. This enzyme hydrolyzed PAF and oxidatively modified phosphatidylcholine. Furthermore, we identified a monomeric polypeptide with a molecular weight of approximately 45 kDa by Western blot using human plasma PAF-AH antibody. These results suggested that plasma type PAF-AH activity exist in CSF taken from children with meningitis.

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.251-257
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• 1995

The objective of the present study was to test the effect of platelet-activating factor (PAF) on rat alveolar macrophages. PAF alone did not stimulate superoxide secretion from alveolar macrophages. However, PAF $(10^{-5}\;M)$ significantly enhanced phagocytic activator zymosan-induced superoxide secretion from alveolar macrophages. This enhancement of PAF plus zymosan was 30% above the sum of the separate effects of PAF and zymosan. Similarly, PAF $1.3{\times}(10^{-5}\;M)$ was not a direct stimulant of alveolar macrophages, as it had no stimulatory effect on chemiluminescence generation, but potentiated zymosan-induced activation of chemiluminescence, i.e., 162% above the separate effects of each stimulant. PAF $10^{-16}{\pm}10^{-6}\;M$ also failed to stimulate IL-1 production from alveolar macrophages. In contrast, when both PAF $10^{-10}\;M$ and lipopolysaccharide(LPS) $(1 {\mu}g/ml)$ were added together at the initiation of the culture, IL-1 production was significantly increased indicating the potentiative effects of PAF on IL-1 production by alveolar macrophages. Collectively, these data suggest that PAF alone does not activate the release of bioactive products from alveolar macrophages. However, PAF appears to act as a priming mediator that potentiates stimuli-induced macrophage activity. These novel actions of PAF prove its role as a potent mediator of inflammatory and immune responses in the lung.

• Korean Journal of Bronchoesophagology
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• v.4 no.2
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• pp.182-187
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• 1998

Platelet activating factor (PAP) has been known as implicating as one of potent inflammatory mediators and reported 0 be involved in inflammation and allergy. PAF induces ciliary dysfunction and epithelial damage of human paranasal sinus mucosa in vitro. However, several recent papers have reported that PAF may not readily damage the airway epithelium. The aim of this study was to investigate the ultrastructural evidence to elucidate the pathogenesis of epithelial damage induced by PAF. Sixteen $\mu\textrm{g}$ g of PAF was applied into the maxillary sinuses of 6 rabbits. Rabbits were divided into 2 subgroups along with time interval at 1st and 3rd experimental day, and sinus mucosae were taken for the histopathologic study using electron microscopy. At 1st day, epithelial cells showed no ultrastructural change. Ultrastructures of the cilia were well preserved. Subepithelial space showed no evidence of the infiltration of inflammatory cells. Intravascular platelet aggregation and swelling of endothelial cells were evident. At 3rd day, epithelial cells showed vacuolar degeneration. Fusion of cilia forming giant cilia and focal loss of cilia were evident. Eosinophils were infiltrated in subepithelial and intraepithelial space. Swelling of endothelial cells, and migration of inflammatory cells into the connective tissue were evident. This study implies that epithelial damage induced by PAF may be secondary to the cytotoxicity of mobilized eosinophils rather than direct cytotoxicity of PAF.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.4
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• pp.415-424
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• 2016

Berberine is an isoquinoline alkaloid found in Rhizoma coptidis, and elicits anti-inflammatory effects through diverse mechanisms. Based on previous reports that activating transcription factor-3 (ATF-3) acts as a negative regulator of LPS signaling, the authors investigated the possible involvement of ATF-3 in the anti-inflammatory effects of berberine. It was found berberine concentration-dependently induced the expressions of ATF-3 at the mRNA and protein levels and concomitantly suppressed the LPS-induced productions of proinflammatory cytokines ($TNF-{\alpha}$, IL-6, and $IL-1{\beta}$). In addition, ATF-3 knockdown abolished the inhibitory effects of berberine on LPS-induced proinflammatory cytokine production, and prevented the berberine-induced suppression of MAPK phosphorylation, but had little effect on AMPK phosphorylation. On the other hand, the effects of berberine, that is, ATF-3 induction, proinflammatory cytokine inhibition, and MAPK inactivation, were prevented by AMPK knockdown, suggesting ATF-3 induction occurs downstream of AMPK activation. The in vivo administration of berberine to mice with LPS-induced endotoxemia increased ATF-3 expression and AMPK phosphorylation in spleen and lung tissues, and concomitantly reduced the plasma and tissue levels of proinflammatory cytokines. These results suggest berberine has an anti-inflammatory effect on macrophages and that this effect is attributable, at least in part, to pathways involving AMPK activation and ATF-3 induction.

• Biomolecules & Therapeutics
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• v.25 no.3
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• pp.337-343
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• 2017

Kahweol as a coffee-specific diterpene has been reported to induce apoptosis in human cancer cells. Although some molecular targets for kahweol-mediated apoptosis have been elucidated, the further mechanism for apoptotic effect of kahweol is not known. Activating transcription factor 3 (ATF3) has been reported to be associated with apoptosis in colorectal cancer. The present study was performed to investigate the molecular mechanism by which kahweol stimulates ATF3 expression and apoptosis in human colorectal cancer cells. Kahweol increased apoptosis in human colorectal cancer cells. It also increased ATF3 expression through the transcriptional activity. The responsible cis-element for ATF3 transcriptional activation by kahweol was CREB located between -147 to -85 of ATF3 promoter. ATF3 overexpression increased kahweol-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by kahweol. Inhibition of ERK1/2 and $GSK3{\beta}$ blocked kahweol-mediated ATF3 expression. The results suggest that kahweol induces apoptosis through ATF3-mediated pathway in human colorectal cancer cells.

• Molecules and Cells
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• v.38 no.1
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• pp.58-64
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• 2015

Activating transcription factor-3 (ATF3) acts as a negative regulator of cytokine production during Gram-negative bacterial infection. A recent study reported that ATF3 provides protection from Streptococcus pneumoniae infection by activating cytokines. However, the mechanism by which S. pneumoniae induces ATF3 after infection is still unknown. In this study, we show that ATF3 was upregulated via Toll-like receptor (TLR) pathways in response to S. pneumoniae infection in vitro. Induction was mediated by TLR4 and TLR2, which are in the TLR family. The expression of ATF3 was induced by pneumolysin (PLY), a potent pneumococcal virulence factor, via the TLR4 pathway. Furthermore, ATF3 induction is mediated by p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Thus, this study reveals a potential role of PLY in modulating ATF3 expression, which is required for the regulation of immune responses against pneumococcal infection in macrophages.