• Proceedings of the SCSK Conference
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• 1999.10a
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• pp.57-64
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• 1999

Pericarpium castaneae extracts have variously potent activities, such as anti-oxidative activity and free radical scavenging activity. in vivo and in vivo studies both indicate that pericarpium castaneae extracts acts as a flee radical scavenger ($IC_{50}$/: 7.6$\mu\textrm{g}$/ml) stronger than gallic acid($IC_{50}$/: 12.5$\mu\textrm{g}$/ml) and ellagic acid($IC_{50}$/: 15$\mu\textrm{g}$/ml) which could prevent cutaneous UV damages and skin aging. The extracts showed a good effect as a anti-oxidant ($IC_{50}$/: 50$\mu\textrm{g}$/ml). It was shown that the appearance of wrinkle in human skin was reduced by topical application of pericarpium castaneae extracts. And the treatment of human skin with the extracts increased the elasticity and moisture of the skin. We investigated the effect of tile pericarpium castaneae extracts on production of extracellular matrix using cultured A431 fibroblast cells. The results indicated that the extracts had no detectable effect on collagen synthesis, But synthesis of cell adhesion protein was increased by the extracts. The results suggest that increase of cell adhesion protein synthesis by pericarpium castaneae extracts has closely related to reduction of wrinkle in skin.

• The Korean Journal of Zoology
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• v.38 no.4
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• pp.457-464
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• 1995

Hela cells, a transformed human epithelial cell line, attach to various substrata but subsequent spreading is specific to collagen or gelatin. The spreading is initiated by the activation of phospholipase $A_2$ (PLA$_2$) which produces arachidonic acid (AA) as a consequence of cell surface collagen receptor clustering. This study examines the mechanism of PLA$_2$activation and which phospholipids are hydrolyzed by PIA$_2$ to release AA in response to Hela cell adhesion to a gelatin substratum. The levels of phosphatidyicholine decreases, among various phospholipids, during attachment and spreading of Hela cells. Lysophosphatidyicholine Is the only lysophospholipids formed during ileLa cell adhesion indicating that clustered collagen receptors activate PLA$_2$to hydrolyze posphatidylcholine to AA and lysophosphatidylcholine. Among various molecular entitles which are known to regulate PLA$_2$ activation, we have previously shown that PLA2 activation is not mediated by either changes in $Ca_2$+ levels, alkalinization of cytoplasmic p11, or activation of protein hinase C. It is also likely that PIA2 activation is not mediated by either pertussis or cholera toxinsensitive G proteins as those toxins do not affect both AA release and cell spreading.

• Journal of Ginseng Research
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• v.41 no.3
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• pp.298-306
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• 2017

Background: Compound K (CK) is a bioactive derivative of ginsenoside Rb1 in Panax ginseng (Korean ginseng). Its biological and pharmacological activities have been studied in various disease conditions, although its immunomodulatory role in innate immunity mediated by monocytes/macrophages has been poorly understood. In this study, we aimed to elucidate the regulatory role of CK on cellular events mediated by monocytes and macrophages in innate immune responses. Methods: The immunomodulatory role of CK was explored by various immunoassays including cell-cell adhesion, fibronectin adhesion, cell migration, phagocytic uptake, costimulatory molecules, reactive oxygen species production, luciferase activity, and by the measurement of mRNA levels of proinflammatory genes. Results: Compound K induced cell cluster formation through cell-cell adhesion, cell migration, and phagocytic activity, but it suppressed cell-tissue interactions in U937 and RAW264.7 cells. Compound K also upregulated the surface expression of the cell adhesion molecule cluster of differentiation (CD) 43 (CD43) and costimulatory molecules CD69, CD80, and CD86, but it downregulated the expression of monocyte differentiation marker CD82 in RAW264.7 cells. Moreover, CK induced the release of reactive oxygen species and induced messenger RNA expression of proinflammatory genes, inducible nitric oxide synthase, and tumor necrosis factor-alpha by enhancing the nuclear translocation and transcriptional activities of nuclear factor kappa-B and activator protein-1. Conclusion: Our results suggest that CK has an immunomodulatory role in innate immune responses through regulating various cellular events mediated by monocytes and macrophages.

• Polymer(Korea)
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• v.27 no.5
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• pp.397-404
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• 2003

The interaction of cell adhesive protein and polypeptide with bone marrow stromal stem cells (BMSCs) grown in tissue engineered films and scaffolds were examined. Several proteins or polypeptide known as cell-adhesive were coated adsorption on poly(lactide-co-glycolide) (PLGA) films and scaffolds and adhesion and proliferation behavior of BMSC on those surfaces were compared. The protein and polypeptide used include collagen IV, fibrinogen, laminin, gelatin, fibronectin, and poly(L-lysine). The protein and polypeptide were adsorbed on the PLGA film surfaces with almost monolayer coverage except poly(L-lysine). BMSCs were cultured for 1, 2, and 4 days on the protein- or polypeptide-adsorbed PLGA films and scaffolds. The cell adhesion and proliferation behaviors were assessed by sulforho damine B assay. It was observed that the protein- or polypeptide-adsorbed surfaces showed better cell adhesion and proliferation than the control.

• Korean Chemical Engineering Research
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• v.47 no.4
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• pp.501-505
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• 2009

In this study, we evaluated the effect of soluble EPCR(Soluble Endothelial Protein C Receptor, sEPCR) on the anti-inflammatory activities by activated protein C(APC) in endothelium. We demonstrated that sEPCR inhibited the barrier protective activity, the inhibition of neutrophils adhesion toward endothelial cells and the inhibition of transendothelial migration by APC in endothelial cells. Interestingly, sEPCR also blocked the mechanism by which APC inhibited the expression of cell adhesion molecules(CAM) by TNF-alpha in endothelial cells. These results suggested that the anti-inflammatory activities of APC was inhibited by sEPCR which blocked the binding motifs of Gla domain of APC to membrane bound EPCR. This finding will provide the important evidence in the development of new medicine for the treatment of severe sepsis and inflammatory diseases and good clue for understanding unknown mechanisms by which APC showed the anti-inflammatory activities in endothelium.

• Archives of Pharmacal Research
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• v.26 no.3
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• pp.244-251
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• 2003

Plant nutrients are believed to provide protection against various diseases including inflammation. Since interactions of the cell adhesion molecules are known to play important roles in mediating inflammation, inhibiting adhesion protein upregulation is a possible therapeutic target. In this study, the interacellular adhesion molecule-1 (ICAM-1) was induced in human umbilical endothelial cells (HUVECs) after stimulation with $TNF-{\alpha}$. In addition, alginate, ascorbic acid and allicin were demonstrated to inhibit the $TNF-{\alpha}$ induced expression of ICAM-1 on the HUVECs in a dose-dependent manner. These compounds also inhibited the production of NO and $H_2O_2$ induced by $TNF-{\alpha}$, which suggests that the inhibition of ICAM-1 expression by the three compounds may be due to the modulated production of the reactive oxygen/nitrogen components. Overall, these results indicate that these dietary components have a therapeutic potential in the treatment of various inflammatory disorders associated with an increase in endothelial leukocyte adhesion molecules.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.229-234
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• 2015

Nafamostat mesilate (NM) is a serine protease inhibitor with anticoagulant and anti-inflammatory effects. NM has been used in Asia for anticoagulation during extracorporeal circulation in patients undergoing continuous renal replacement therapy and extra corporeal membrane oxygenation. Oxidative stress is an independent risk factor for atherosclerotic vascular disease and is associated with vascular endothelial function. We investigated whether NM could inhibit endothelial dysfunction induced by tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$ ). Human umbilical vein endothelial cells (HUVECs) were treated with TNF-${\alpha}$ for 24 h. The effects of NM on monocyte adhesion, vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) protein expression, p38 mitogenactivated protein kinase (MAPK) activation, and intracellular superoxide production were then examined. NM ($0.01{\sim}100{\mu}g/mL$) did not affect HUVEC viability; however, it inhibited the increases in reactive oxygen species (ROS) production and p66shc expression elicited by TNF-${\alpha}$ (3 ng/mL), and it dose dependently prevented the TNF-${\alpha}$ -induced upregulation of endothelial VCAM-1 and ICAM-1. In addition, it mitigated TNF-${\alpha}$ -induced p38 MAPK phosphorylation and the adhesion of U937 monocytes. These data suggest that NM mitigates TNF-${\alpha}$ -induced monocyte adhesion and the expression of endothelial cell adhesion molecules, and that the anti-adhesive effect of NM is mediated through the inhibition of p66shc, ROS production, and p38 MAPK activation.

• Fisheries and Aquatic Sciences
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• v.22 no.3
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• pp.7.1-7.10
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• 2019

Sargassum serratifolium ethanolic extract has been known for strong antioxidant and anti-inflammatory properties. We prepared hexane fraction from the ethanolic extract of S. serratifolium (HSS) to improve biological activities. In this study, we investigated the effects of HSS on the inhibition of tumor necrosis factor (TNF)-${\alpha}$-induced monocyte adhesion to human umbilical vein endothelial cells (HUVECs). We found that HSS suppressed the production of cell adhesion molecules such as intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 in TNF-${\alpha}$-induced HUVECs. Moreover, TNF-${\alpha}$-induced production of monocyte chemoattractant protein 1 and keratinocyte chemoattractant was inhibited by HSS treatment. HSS suppressed TNF-${\alpha}$-induced nuclear factor kappa B ($NF-{\kappa}B$) activation via preventing proteolytic degradation of inhibitor ${\kappa}B-{\alpha}$. HSS induced the production of heme oxygenase 1 via translocation of Nrf2 into the nucleus in TNF-${\alpha}$-treated HUVECs. Overall, HSS alleviated vascular inflammation through the downregulation of $NF-{\kappa}B$ activation and the upregulation of Nrf2 activation in TNF-${\alpha}$-induced HUVECs. These results indicate that HSS may be used as therapeutic agents for vascular inflammatory disorders.

• Korean Journal of Microbiology
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• v.47 no.4
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• pp.348-355
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• 2011

Staphylococcus aureus is a major human pathogen that is associated with various types of local and systemic infection. Staphylococcal protin A (SPA), a highly expressed surface component of S. aureus, may have a role in virulence such as activating inflammation and interfering with immune clearance. We examined the effect of recombinant SPA on inflammatory response in human HaCaT keratinocytes. The recombinant SPA protein was prepared using the pET-28a Vector System in Escherichia coli. The expression of pro-inflammatory related adhesion molecules and cytokines in HaCaT cells incubated for 6, 12, and 24 h with SPA (2 ${\mu}g$/ml) was analyzed by comparative RT-PCR or ELISA. The expression of E-selectin, ICAM-1, MCP-1, IL-6 and IL-8 was significantly increased in HaCaT from 6 to 24 h after treatment with SPA. SPA showed the effect on the adhesion-promoting ability of U937 monocytes to HaCaT cells. Our data demonstrate that SPA stimulates inflammatory response of HaCaT cells, implicating an important factor for exacerbation of skin inflammation of immunologic disease.

• Korean Journal of Environmental Biology
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• v.27 no.1
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• pp.88-94
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• 2009

The process of atherosclerosis begins through secretion of inflammatory cytokine or adhesion of leukocyte from damage in blood vessels and transmigration. This study was conducted to investigate the effects of delphinidin chloride (DC) in the initial process of atherosclerosis on the expression of ICAM-1 (Intracellular Adhesion Molecule-1) and VCAM-1 (Vascular Adhesion Molecule-1) related to adhesion of leukocyte at the HUVEC (human umbilical vein endothelial cell line. As a result, cell growth inhibition rate at 50 ${\mu}M$ was respectively 4, 3 and 5% without cell toxicity. As a result of morphological observation monocyte-endothelial cell adhesion assay and optical microscope carried out to measure attachment of mononuclear cells to endothelial cells induced by Tumor necrosis factor-alpha (TNF-$\alpha$) at concentrations without cell toxicity, DC concentration-dependently suppressed attachment. When effects on the expression of VCAM-1 and ICAM-1, cell adhesion molecules induced from endothelial cells by TNF-$\alpha$, were comparatively analyzed using western blot analysis and RT-PCR methods, protein of VCAM-1 and ICAM-1 and expression at the level of mRNA were concentration-dependently reduced. Taken together, the results of this studies provide evidence that DC possess an anti-metastatic activity.