• Korean Circulation Journal
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• v.53 no.2
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• pp.92-102
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• 2023

Background and Objectives: YKL-40 is considered to be associated with cardiovascular disease (CVD). In this study, the effect of serum 25(OH) vitamin D [25(OH)VitD] differences between groups on YKL-40 was evaluated on a hypercholesterolemia rat model. Methods: Thirty-two male rats (wistar albino) were equally divided into 4 groups. The first group was the control group; the second group was high-cholesterol (H-CH) adequate vitamin D (VitD) group (H-Ade^VD). The third group was the H-CH deficient VitD group (H-Def^VD), and the last group was designed with the H-CH supplement VitD (H-Sup^VD). The feeding process consisted of 2 stages. At the first stage (5 months), the H-Def^VD group was fed on VitD deficient chow, while the other groups (control, H-Ade^VD, H-Sup^VD) were fed on standard chow. At the second stage (3 months), the H-Ade^VD and the H-Sup^VD groups were fed on the H-CH chow, whereas the H-Def^VD group was fed on the H-CH-VitD deficient chow. Moreover, the H-Sup^VD group was given 100 IU/kg/day VitD along with the H-CH chow. Results: Compared with the control group, interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and YKL-40 values in the H-Def^VD groups increased significantly (p<0.001, p<0.001, p=0.009, p=0.005; sequentially). Conclusion: It can be concluded that VitD can suppress the YKL-40, thus, it will prevent CVD development in rat. Therefore, further clinical studies related with human will reveal the effect of VitD and YKL-40 on CVD development.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2004.04a
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• pp.61-77
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• 2004

Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum(Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CC14), D-galactosamine (DGal) and Bacillus Calmette-Guerin(BCG) plus lipopolysaccharides(LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts(AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-l (ICAM-1) and vascular cell adhesion molecule-l (VCAM-1) induced by ox-LDL and AGE.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.109-115
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• 2005

Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD(P)H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 ($3.5{\pm}0.4$) and VCAM-1 ($3.8{\pm}0.3$) in diabetic aorta was significantly higher than those in control aorta ($0.9{\pm}0.5$ and $1.6{\pm}0.3$, respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD(P)H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P＜0.01 in ICAM-1 and r=0.88, P＜0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD(P)H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.4
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• pp.217-222
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• 2006

Atherosclerosis is considered as a chronic inflammatory process. However, the nature of the oxidant signaling that regulates monocyte adhesion and its underlying mechanism is poorly understood. We investigated the role of reactive oxygen species on the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion in the cultured endothelial cells. $TNF-{\alpha}$ at a range of $1{\sim}30\;ng/ml$ induced VCAM-1 expression dose-dependently. BCECF-AM-labeled U937 cells firmly adhered on the surface of endothelial cells when the endothelial cells were incubated with $TNF-{\alpha}$ (15 ng/ml). Ten $\;{\mu}mol/L$ of SB203580, an inhibitor of p38 MAPK, significantly reduced $TNF-{\alpha}-induced$ VCAM-1 expression, compared to the JNK inhibitor ($40\;{\mu}mol/L$ of SP60015) or ERK inhibitor ($40\;{\mu}mol/L$ of U0126). Also, SB203580 significantly inhibited $TNF-{\alpha}-induced$ monocyte adhesion in HUVEC. Superoxide production was minimal in the basal condition, however, treatment of $TNF-{\alpha}$ induced superoxide production in the dihydroethidineloaded endothelial cells. Diphenyleneiodonium (DPI, $10\;{\mu}mol/L$), an inhibitor of NADPH oxidase, and rotenone $(1\;{\mu}mol/L)$, an inhibitor of mitochondrial complex I inhibited $TNF-{\alpha}-induced$ superoxide production, VCAM-1 expression and monocyte adhesion in the endothelial cells. Taken together, our data suggest that NADPH oxidase and mitochondrial ROS were involved in $TNF-{\alpha}-induced$ VCAM-1 and monocyte adhesion in the endothelial cells.

• Journal of Periodontal and Implant Science
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• v.26 no.3
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• pp.655-668
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• 1996

The change in vascular adhesion molecule expression and number of infiltrating leukocytes were investigated irnmunohistochemically in clinically healthy and inflammed gingiva. Monoclonal antibodies to ICAM-1, VCAM-1 and E-cadherin were used to identify positive vessels and leukocyte within gingival biopsies. 10 healthy gingiva and 30 inflammed gingiva was resected by clinical crown lengthening and modified Widman flap operation, respectively. Leukocyte entry into tissues at sites of inflammation is controlled by the interaction between adhesion molecule and endothelium. Because of rapid and severe destructive periodontal disease that is remarkable leukocyte adhesion deficiency, it is very important to unerdstand the mechanism of host defence against periodontal disease. The purpose of this investigation was the characterization of the presence and distribution of the adhesion molecule(ICAM-1, VCAM-1 and Evcadherin) in inflammatory gingival tissues compared to clinically healthy gingiva. The results were as followed; 1. ICAM-1 was distributed on basal layer, endothelium and mononuclear cells 10 healthy gingiva but inflammed gingiva was observed stronger stain than healthy gingiva. 2. Rare expression was observed in both group but few positive VCAM-1 cells were investigated in inflammatory gingival tissues 3. E-cadherin was expressed in only epithelium and reduced expression was observed in inflammatory gingival tissues. ICAM-1, VCAM-1 showed more expression in inflammatory tissues compared to healthy gingiva. Conversely, E-cadherin revealed a opposite result. These finding demonstrate a characteristic distribution and degree of adhesion molecule in healthy and inflammatory gingival tissues. But it is suggested that more detail study be progressive associated with leukocyte adhesion molecule to determine characterization of periodontal disease.

• The Journal of Korean Obstetrics and Gynecology
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• v.32 no.3
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• pp.20-31
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• 2019

Objectives: The seeds from Arctium lappa have been considered for its various pharmacological properties, which include anti-carcinogenic, anti-inflammatory, anti-diabetic, and anti-viral activities. Methods: In the present study, we investigated the anti-inflammatory effect of the ethanol extract from the seeds of Arctium lappa L (EAL) on cytokine-induced vascular inflammation in human umbilical vein endothelial cells (HUVEC). Results: Pretreatment with EAL significantly decreased tumor necrosis factor alpha ($TNF-{\alpha}$)-induced cell adhesion molecules expression such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial-selectin (E-selectin) in a dose-dependent manner. Cell adhesion assay showed that pretreatment with EAL suppressed HUVEC-monocyte adhesion by $TNF-{\alpha}$ over $1{\mu}g/ml$ concentration. We investigated the involvement of nuclear transcription factor kappa-B ($NF-{\kappa}B$) in $TNF-{\alpha}$-induced vascular inflammation. $NF-{\kappa}B$ p65 nuclear expression was induced by $TNF-{\alpha}$, however, pretreatment with EAL was attenuated that nuclear translocation. In cytoplasm, EAL was also attenuated $TNF-{\alpha}$-induced decrease of inhibitor of ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$) expression. Moreover, EAL significantly decreased $TNF-{\alpha}$-induced production of intracellular reactive oxygen species (ROS). Conclusions: Taken together, our findings suggest that seeds of Arctium lappa L could be a therapeutic herb for prevention of cardiovascular diseases throughout the inhibition of vascular endothelial inflammation.

• IMMUNE NETWORK
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• v.2 no.1
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• pp.6-11
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• 2002

Background: Inflammation is a frequent reaction following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface is known to be associated with inflammation, the expression of adhesion molecules is an important therapeutic target. Methods: Treatment of human umbilical endothelial cells (HUVECs) with ${\gamma}$-irradiation (${\gamma}IR$) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Changes in the expression of these proteins on ${\gamma}$-irradiated HUVECs which had been treated previously with allicin were measured by ELISA. Results: In the present study, we demonstrate that allicin inhibits the ${\gamma}IR$ induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose-dependent manner. Allicin was also found to inhibit the ${\gamma}IR$ induced production of nitric oxide (NO). Conclusion: These data suggest that allicin has a therapeutic potential for the treatment of various inflammatory disorders associated with increase numbers of endothelial leukocyte adhesion molecules.

• BMB Reports
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• v.46 no.7
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• pp.352-357
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• 2013

Atherosclerosis, which manifests as acute coronary syndrome, stroke, and peripheral arterial diseases, is a chronic inflammatory disease of the arterial wall. Prunella vulgaris, a perennial herb with a worldwide distribution, has been used as a traditional medicine in inflammatory disease. Here, we investigated the effects of P. vulgaris ethanol extract on TNF-${\alpha}$-induced inflammatory responses in human aortic smooth muscle cells (HASMCs). We found that P. vulgaris ethanol extract inhibited adhesion of monocyte/macrophage-like THP-1 cells to activated HASMCs. It also decreased expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and ROS, No production in TNF-${\alpha}$-induced HASMCs and reduced NF-${\kappa}B$ activation. Furthermore, P. vulgaris extract suppressed TNF-${\alpha}$-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK). These results demonstrate that P. vulgaris possesses anti-inflammatory properties and can regulate TNF-${\alpha}$-induced expression of adhesion molecules by inhibiting the p38 MAPK/ERK signaling pathway.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1152-1156
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• 2007

The Camella japonica flower(CJF) extract was studied for their anti-angiogenenic and anti-cell adhesion effect. CJF-extract inhibited the tube formation on human umbilical vein endotherial cells(HUVEC) with butanol extract by 70.2%, acetone extract by 54.2%, ethyl acetate extract by 37.0%, chloroform extract by 21.2%. Cell adhesion molecules were effectively suppressed at different concentration of CJF at 50, 100, 200 ug/well such as for intercellular adhesion molecule(ICAM) by 5.9%, 29.4% and 52.9%, for vascular cell adhesion molecule(VCAM) by 12.5%, 43.8% and 62.5%, for E-selectin by 7.1%, 21.4% and 35.7%, respectively. Signal molecules of vascular endotherial growth factor receptor 2(VEGFR2), ${/beta}$-catenin and PI3K are inhibited by different concentration of CJF at 10, 20 and 30 ${\mu}g/mL$ with western blot. Angiogenesis will be inhibited with suppressing NF-kB molecule resulted in signal molecules blocked by CJF. CJF will be useful materials for treatment of angiogenesis related diseases such as cancer, metastasis, rheumathioid arthritis and obesity.

• Biomolecules & Therapeutics
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• v.9 no.3
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• pp.156-161
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• 2001

Inflammation is a frequent radiation-induced following therapeutic irradiation. Treatment of human umbilical endothelial cells (HUVEC) with ${\gamma}$-irradiation (${\gamma}$IR) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Since the upregulation of these proteins on endothelial cell surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. In the present study, we demonstrate that bioflavonoid rutin inhibits ${\gamma}$IR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose- and time dependent manner. Rutin also inhibited ${\gamma}$IR induced production of NO. These data suggest that rutin has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.