• 제목/요약/키워드: Vascular adhesion molecule

검색결과 101건 처리시간 0.027초

Inhibitory Effects of Licochalcone A and Isoliquiritigenin on Monocyte Adhesion to TNF-$\alpha$-activated Endothelium

  • Kwon Hyang-Mi;Lim Soon Sung;Choi Yean-Jung;Jeong Yu-Jin;Kang Sang-Wook;Bae Ji-Young;Kang Young-Hee
    • Nutritional Sciences
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    • 제8권3호
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    • pp.153-158
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    • 2005
  • Numerous natural herbal compounds have been reported to inhibit adhesion and migration of leukocytes to the site of inflammation Licorice extracts, which have been widely used in traditional Chinese medicinal preparation, possess various pharmacological effects. Isoliquiritigenin, a biogenetic precursor of flavonoids with various pharmacological effects, is a natural pigment present in licorice. We attempted to explore whether licorice extracts and isoliquiritigenin mitigate monocyte adhesion to tumor necrosis factor-$\alpha$ (TNF-$\alpha$)-activated human umbilical vein endothelial cells (HUVEC). In addition, it was tested whether the inhibition of monocyte adhesion to the activated HUVEC accompanied a reduction in vascular cell adhesion molecule-l expression(VCAM-l). Dry-roasted licorice extracts in methylene chloride but not in ethanol markedly interfered with THP-l monocyte adhesion to INF-$\alpha$-activated endothelial cells. licochalcone A compound isolated from licorice extract in methylene chloride appeared to modestly inhibit the interaction of THP-l monocytes and activated endothelium. In addition, isoliquiritigenin abolished the monocyte adhesion with attenuating VCAM-l protein expression on HUVEC induced by INF-$\alpha$. These results demonstrated that non-polar components from dry-roasted licorice extracts containing licochalcone A as well as isoliquiritigenin were active in blocking monocyte adhesion to cytokine-activated endothelimn, which appeared to be mediated most likely through the inhibition of VCAM-l expression on HUVEC. Therefore, licorice may hamper initial inflammatory events on the vascular endothelium involving induction of endothelial cell adhesion molecules.

염증성 치은조직에서 Cell Adhesion Molecule의 발현에 관한 연구 (Expression of Adhesion Molecule in Inflammatory Gingival Tissue)

  • 박경근;김은철;유형근;신형식
    • Journal of Periodontal and Implant Science
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    • 제26권3호
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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.

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고지혈증 동물모델에서 홍삼과 천마 혼합투여에 의한 혈관 염증 개선연구 (Combination with Korean Red Ginseng and Gastrodia rhizoma Enhances Vascular Protective Effects in Hyperlipidemic Rats)

  • 이윤정;김혜윰;윤정주;이소민;고정현;이호섭;최경민;강대길
    • 대한한의학방제학회지
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    • 제20권1호
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    • pp.1-11
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    • 2012
  • Objectives : This experimental study was designed to investigate the inhibitory effects of combination with Korean red ginseng and Gastrodia rhizoma on vascular dysfunction in high-fat/cholesterol diet-induced hyperlipidemia. Methods : Sprague-Dawley rats were fed with 7.5% cocoa butter and 1.25% cholesterol for 10 weeks, with Panax ginseng (PG), and mixtures of Panax ginseng and Gastrodia rhizoma (PGM), respectively. Results : Chronic treatment with PG and PGM significantly decreased body weight. The aortic expression of cell adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin were markedly increased in hyperlipidemia rats. Interestingly, PGM significantly decreased cell adhesion molecules expression. However, there was no significant decrease in PG group. In addition, PG and PGM group inhibited high-fat/cholesterol diet-induced cytokine such as monocyte chemoattractant protein (MCP-1) mRNA expression. Furthermore, PG and PGM group significantly decreased c-reactive protein protein (CRP) level. Especially, PGM significantly accentuated the decrease of MCP-1 mRNA expression and CRP level. Conclusions : the present study provides an evidence that combination with Panax ginseng and Gastrodia rhizoma enhances anti-vascular protective effects through suppression of vascular inflammation in hyperlipidemic rats.

혈관내피세포에서 TNF-$\alpha$ 자극에 의해 유도되는 혈관염증에 대한 WK-38의 억제 효과 (Inhibitory Effect of WK-38 on TNF-$\alpha$ Induced Vascular Inflammation in Human Umbilical Vein Endothelial Cells)

  • 황선미;이윤정;김은주;윤정주;이혁;강대길;이호섭
    • 동의생리병리학회지
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    • 제23권5호
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    • pp.1132-1138
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    • 2009
  • Vascular inflammation is an important event in the development of vascular diseases such as tumor progression and atherosclerosis. This study was to investigate the inhibitory effects of WK-38, a new herbal prescription for the treatment of atherosclerosis, on vascular inflammation in human umbilical vein endothelial cells (HUVEC). WK-38 is composed of Rhei Rhizoma, Magonoliae Cortex, Moutan Cortez Radicis. Pretreatment with WK-38 was significantly blocked TNF-$\alpha$-induced expression level of cell adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), and endothelial cell selectin (E-selectin) in a dose-dependent manner. TNF-$\alpha$-induced cell adhesion in co-cultured U937 and HUVEC was also blocked by pretreatment with WK-38. Moreover, WK-38 significantly suppressed p65 NF-${\kappa}B$ translocation into the nucleus by TNF-$\alpha$ as well as the phosphorylation and degradation of $I{\kappa}B-{\alpha}$. In conclusion, the present data suggested that WK-38 could suppress TNF-$\alpha$-induced vascular inflammatory process, though inhibition of NF-${\kappa}B$ activation in HUVEC.

The protective effect of Prunella vulgaris ethanol extract against vascular inflammation in TNF-α-stimulated human aortic smooth muscle cells

  • Park, Sun Haeng;Koo, Hyun Jung;Sung, Yoon Young;Kim, Ho Kyoung
    • BMB Reports
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    • 제46권7호
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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.

유향 추출물이 혈관내피세포 부착단백질 발현에 미치는 영향 (Effects of Olibanum Extracts on Vascular Cell Adhesion Molecules Expression)

  • 이숭인;권강범;한종현;류도곤
    • 동의생리병리학회지
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    • 제25권3호
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    • pp.445-450
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    • 2011
  • In order to validate the use of Olibanum as an anti-inflammatory drug in the traditional Korean medicine, I have investigated the effect of water-soluble extract of Olibanum (EO) on the expression of pro-inflammatory vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-${\alpha}$. The extract inhibited dose-dependently VCAM-1 expression without its cytotoxic effect on HUVECs, as measured by a flow cytometer using fluorescence-enhanced anti-VCAM-1 antibody, and significantly decreased mRNA levels of VCAM-1, as determined using reverse transcription polymerase chain reaction. These results suggest that Olibanum may have therapeutic potential in the control of endothelial disorders caused by inflammation.

Manassantin A and B Isolated from Saururus chinensis Inhibit $TNF-{\alpha}-Induced$ Cell Adhesion Molecule Expression of Human Umbilical Vein Endothelial Cells

  • Kwon Oh Eok;Lee Hyun Sun;Lee Seung Woong;Chung Mi Yeon;Bae Ki Hwan;Rho Mun-Chual;Kim Young-kook
    • Archives of Pharmacal Research
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    • 제28권1호
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    • pp.55-60
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    • 2005
  • Leukocyte adhesion to the vascular endothelium is a critical initiating step in inflammation and atherosclerosis. We have herein studied the effect of manassantin A (1) and S (2), dineolignans, on interaction of THP-1 monocytic cells and human umbilical vein endothelial cells (HUVEC) and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in HUVEC. When HUVEC were pretreated with 1 and 2 followed by stimulation with $TNF-{\alpha}$, adhesion of THP-1 cells to HUVEC decreased in dose-dependent manner with $IC_{50}$ values of 5 ng/mL and 7 ng/mL, respectively, without cytotoxicity. Also, 1 and 2 inhibited $TNF-{\alpha}-induceda$ up-regulation of ICAM-1, VCAM-1 and E-selectin. The present findings suggest that 1 and 2 prevent monocyte adhesion to HUVEC through the inhibition of ICAM-1, VCAM-1 and E-selectin expression stimulated by $TNF-\alpha$, and may imply their usefulness for the prevention of atherosclerosis relevant to endothelial activation.

마우스 대식세포 및 사람 혈관 내피세포에서 오수유(Evodia officinalis $D_{ODE}$) 메탄올 추출물의 항염증 효과 (Anti-inflammatory Effect of Evodia Officinalis $D_{ODE}$ in Mouse Macrophage and Human Vascular Endotherial Cells)

  • 윤현정;허숙경;이영태;박원환;박선동
    • 대한본초학회지
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    • 제23권1호
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    • pp.29-38
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    • 2008
  • Objectives : Evodia officinalis DODE (EO), an herbal plant, has been widely used in traditional Korean medicine for the treatment of vascular diseases such as hypertension. The crude extract of EO contains phenolic compounds that are effective in protecting liver microsomes, hepatocytes, and erythrocytes against oxidative damage. But EO has been little found to have an anti-inflammatory activity. We investigated anti-inflammatory activity of EO in RAW 264.7 cells and human umbilical vein endothelial cells (HUVECs). Methods : Cytotoxic activity of EO on RAW 264.7 cells was investigated by using 5-(3-caroboxymeth-oxyphenyl)-2H-tetra-zolium inner salt (MTS) assay. The nitric oxide (NO) production was measured by Griess reagent system. And proinflammatory cytokines were measured by ELISA kit. The levels of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression were measured by flow cytometer. Results : EO decreased LPS-induced NO production in RAW 264.7 cells. The inhibitory activity of EO on LPS-induced NO release is probably associated with suppressing TNF-${\alpha}$, IL-6 and MCP-1 formation. These results indicate that EO has potential as an anti-inflammatory agent. Moreover, EO decreased TNF-${\alpha}$-induced IL-8, IL-6 production, and ICAM-1 and VCAM-1 expression in HUVECs. Conclusions : EO inhibits TNF-${\alpha}$-induced inflammation via decreasing cytokines production and adhesion molecules expression. These results indicate that EO has potential as an anti-inflammation and anti-artherosclerosis agent.

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γ-Irradiation Induced Adhesion Molecules are Reduced by Vitamin C in Human Endothelial Cells

  • Son, Eun-Wha;Kim, Byung-Oh;Pyo, Suh-Kneung
    • Biomolecules & Therapeutics
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    • 제12권3호
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    • pp.145-150
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    • 2004
  • Inflammation is a frequent radiation-induced reaction 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 vitamin C inhibits ${\gamma}$IR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose- and time dependent manner. Vitamin C a1so inhibited the production of Nitric oxide (NO) induced by ${\gamma}$IR. These data suggest that vitamin C has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.