• Natural Product Sciences
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• v.11 no.3
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• pp.131-135
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• 2005

Methanolic extracts of ninety-five medicinal plants were screened for platelet-activating factor (PAF) receptor binding inhibitory activity using rabbit platelet. Alpinia officinarum, Belamcanda chinensis, Leonurus heterophyllus, Pinus densiflora, Polygonatum sibiricum and Sambucus williamsii showed significant inhibitory effects on the platelet-activating factor (PAF) receptor binding.

• Natural Product Sciences
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• v.2 no.2
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• pp.86-89
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• 1996

Methanolic extracts of 25 species of Malaysian medicinal plants were screened for platelet-activating factor (PAF) receptor binding activity using rabbit platelet. Extracts of Cinnamomum sintoc, Ixonanthes iconsandra, Paederia foetida, Piper aduncum, Premna integrifolia, Ardisia crispa, and Ardisia elliptica showed significant inhibitory effect on the platelet-activating factor (PAF) receptor binding.

• Korean Journal of Medicinal Crop Science
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• v.13 no.4
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• pp.178-181
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• 2005

Methanolic extracts of fifteen Chinese medicinal plants were screened for platelet-activating factor (PAF) receptor binding inhibitory activity using rabbit platelet. Campsis grandiflora, Dalbergia odorifera, Vaccaria segetalis and Zanthoxylum nitidum showed significant inhibitory effects on the platelet-activating factor (PAF) receptor binding. Campsis grandiflora, Dalbergia odorifera, Vaccaria segetalis and Zanthoxylum nitidum inhibited 52%, 56%, 70%, and 66% respectively at the concentration of 0.2 mg/ml.

• 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.

• Clinical and Experimental Reproductive Medicine
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• v.18 no.2
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• pp.143-151
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• 1991

An embryo-derived platelet activating factor (PAF) has been demonstrated to play an important role in reproduction. This report examined the effect of PAF on ovulation, fertilization, embryo development, implantation and fetal viability by using murine model. PAF had no stimulatory effect on ovulation and fertilization. But PAF had stimulatory effect on embryo development in in-vitro test, in spite of no effect on implantation and fetal viability. These results demonstrate that exogenous PAF could enhance embryo development and implantation and give suggestion that PAF may play an role in human IVF program.

• Journal of Microbiology and Biotechnology
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• v.16 no.8
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• pp.1292-1300
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• 2006

Aeromonas encheleia, a potential human intestinal pathogen, was shown to infect a human intestinal epithelial cell line (Caco-2) in a noninvasive manner. The transcriptional profile of the Caco-2 cells after infection with the bacteria revealed an upregulated expression of genes involved in chloride secretion, including that of phospholipase A2 (PLA2) and platelet-activating factor (PAF) acetylhydrolase (PAFAH2). This was also confirmed by a real-time RT-PCR analysis. As expected from PLA2 induction, PAF was produced when the Caco-2 cells were infected with the bacteria, and PAF was also produced when the cells were treated with a bacterial culture supernatant including bacterial extracellular proteins, yet lacking lipopolysaccharides. Bacterial aerolysin was shown to induce the production of PAF.

• Korean Journal of Pharmacognosy
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• v.25 no.2
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• pp.167-170
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• 1994

The platelet activating factor (PAF) is a newly discovered chemical mediator, the chemical structure of which is 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine. Since PAF has potent and broad activities, its pathophysiological roles have received much attention. To develope a new PAF antagonist from medicinal plants, extracts of twenty medicinal herb were screened using PAF receptor binding, $[^{14}C]$ serotonin release and platelet aggregation.

• 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.

• 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 Pharmacology
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• v.32 no.1
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• pp.103-112
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• 1996

Roles of protein kinase C and protein tyrosine kinase in the activation of neutrophil respiratory burst, degranulation and elevation of cytosolic $Ca^{2+}$ in platelet-activating factor (PAF)-stimulated neutrophils were investigated. Superoxide and $H_2O_2$ production and myeloperoxidase and acid phosphatase release in PAF-stimulated neutrophils were inhibited by protein kinase C inhibitors, staurosporine and H-7 and protein tyrosine kinase inhibitors, genistein and tyrphostin. The PAF-induced elevation of $[Ca^{2+}]_i$ in neutrophils was inhibited by staurosporine, genistein and methyl-2,5-dihydroxycinnamate. Staurosporine inhibited both intracellular $Ca^{2+}$ release and $Mn^{2+}$ influx in PAF-stimulated neutrophils. Genistein and methyl-2,5-dihydroxycinnamate inhibited $Mn^{2+}$ influx induced by PAF, whereas their effects on intracellular $Ca^{2+}$ release were not detected. In neutrophils preactivated by PMA, the stimulatory effect of PAF on the elevation of $[Ca^{2+}]_i$ was reduced. Protein kinase C and protein tyrosine kinase may be involved in respiratory burst, lysosomal enzyme release and $Ca^{2+}$ mobilization in PAF-stimulated neutrophils. The elevation of $[Ca^{2+}]_i$ appears to be accomplished by intracullular $Ca^{2+}$ release and $Ca^{2+}$ influx which are differently regulated by protein kinases. Preactivation of protein kinase C appears to attenuate the stimulatory action of PAF on intracellular $Ca^{2+}$ mobilization.