• Title, Summary, Keyword: HUVECs

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Hexane fraction from the ethanolic extract of Sargassum serratifolium suppresses cell adhesion molecules via regulation of NF-κB and Nrf2 pathway in human umbilical vein endothelial cells

  • Gwon, Wi-Gyeong;Lee, Sang-Gil;Kim, Jae-Il;Kim, Young-Mog;Kim, Seon-Bong;Kim, Hyeung-Rak
    • 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.

Puerariae Radix Induces Angiogenesis in vitro and in vivo

  • Choi, Do-Young;Kang, Jung-Won;Cho, Eun-Mi;Lee, Jae-Dong;Huh, Jeong-Eun;Yang, Ha-Ru;Baek, Yong-Hyeon;Kim, Deog-Yoon;Cho, Yoon-Je;Kim, Kang-Il;Park, Dong-Suk
    • Journal of Acupuncture Research
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    • v.22 no.2
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    • pp.171-180
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    • 2005
  • Background & Objective : Angiogenesis consists of the proliferation, migration, and differentiation of endothelial cells, and angiogenic factors and matrix protein interactions modulate this process. The aim of this study was to determine whether Puerariae radix could induce angiogenic activity in human umbilical vein endothelial cells (HUVECs). Methods: The angiogenic activity of Puerariae radix were evaluated by using BrdU assay, chemotactic migration assay, tube formation assay, measurement of bFGF in HUVECs, and Matrigel plug assay in mice. Results : Puerariae radix significantly increased HUVECs proliferation in a dose-dependent manner. In addition, Puerariae radix increased migration and tube-like formation in HUVECs. Interestingly,the expression of basic fibroblast growth factor (bFGF), an angiogenesis-stimulating growth factor, was dose-dependently increased by Puerariae radix. The angiogenic activity of Puerariae radix was confirmed using an in vivo Matrigel angiogenesis model, showing promotion of blood vessel formation. Conclusion : Puerariae radix significantly induces angiogenesis in vitro and in vivo. These results suggest that Puerariae radix is a potent angiogenic agent, and a promising drug, for the induction of neovascularization.

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A standardized bamboo leaf extract inhibits monocyte adhesion to endothelial cells by modulating vascular cell adhesion protein-1

  • Choi, Sunga;Park, Myoung Soo;Lee, Yu Ran;Lee, Young Chul;Kim, Tae Woo;Do, Seon-Gil;Kim, Dong Seon;Jeon, Byeong Hwa
    • Nutrition Research and Practice
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    • v.7 no.1
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    • pp.9-14
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    • 2013
  • Bamboo leaves (Phyllostachys pubescens Mazel ex J. Houz (Poacea)) have a long history of food and medical applications in Asia, including Japan and Korea. They have been used as a traditional medicine for centuries. We investigated the mechanism of anti-inflammatory activity of a bamboo leaf extract (BLE) on tumor necrosis factor-alpha (TNF-${\alpha}$)-induced monocyte adhesion in human umbilical vein endothelial cells (HUVECs). Exposure of HUVECs to BLE did not inhibit cell viability or cause morphological changes at concentrations ranging from 1 ${\mu}g/ml$ to 1 mg/ml. Treatment with 0.1 mg/ml BLE caused 63% inhibition of monocyte adhesion in TNF-${\alpha}$-activated HUVECs, which was associated with 38.4% suppression of vascular cell adhesion molecule-1 expression. Furthermore, TNF-${\alpha}$-induced reactive oxygen species generation was decreased to 47.9% in BLE treated TNF-${\alpha}$-activated HUVECs. BLE (0.05 mg/ml) also caused about 50% inhibition of interleukin-6 secretion from lipopolysaccharide-stimulated monocyte. The results indicate that BLE may be clinically useful as an anti-inflammatory or anti-oxidant for human cardiovascular disease including atherosclerosis.

Comparative effect of genistein and daidzein on the expression of MCP-l, eNOS, and cell adhesion molecules in TNF-${\alpha}$-stimulated HUVECs

  • Cho, Hye-Yeon;Park, Chung-Mu;Kim, Mi-Jeong;Chinzorig, Radnaabazar;Cho, Chung-Won;Song, Young-Sun
    • Nutrition Research and Practice
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    • v.5 no.5
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    • pp.381-388
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    • 2011
  • We compared the effects of genistein and daidzein on the expression of chemokines, cell adhesion molecules (CAMs), and endothelial nitric oxide synthase (eNOS) in tumor necrosis factor (TNF)-${\alpha}$-stimulated human umbilical vascular endothelial cells (HUVECs). TNF-${\alpha}$ exposure significantly increased expression of monocyte chemoattractant protein (MCP)-l, vascular adhesion molecule (VCAM)-1, and intercellular adhesion molecule-1. Genistein significantly decreased MCP-l and VCAM-l production in a dose-dependent manner, whereas CAM expression was not significantly lowered by genistein treatment. However, daidzein slightly decreased MCP-l production. The effects of genistein and daidzein on MCP-l secretion coincided with mRNA expression. Pre-treatment with either genistein or daidzein elevated eNOS expression and nitric oxide production disturbed by TNF-${\alpha}$ exposure. A low concentration of isoflavones significantly inhibited nuclear factor (NF)${\kappa}$B activation, whereas a high dose slightly ameliorated these inhibitive effects. These results suggest that genistein had a stronger effect on MCP-l and eNOS expression than that of daidzein. Additionally, NF${\kappa}$B transactivation might be partially related to the down-regulation of these mRNAs in TNF-${\alpha}$-stimulated HUVECs.

Effects of Faeces Trogopterori on the Production of Chemokine in HUVECs (오령지 물추출물이 혈관내피세포의 chemokine 생성에 미치는 영향)

  • Moon, Chang-Min;Kwon, Kang-Beom;Ryu, Do-Gon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.24 no.5
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    • pp.822-826
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    • 2010
  • In order to validate the use of Faeces Trogopterori as an anti-inflammatory drug in the traditional Korean medicine, I have investigated the effect of water-soluble extract of F. Trogopterori (EFT) on the production of monocyte chemoattractant protein-1 (MCP-1), of which chemokine stimulates the migration of mononuclear cells, in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-alpha. The extract inhibited dose-dependently MCP-1 production without its cytotoxic effect on HUVECs, as measured by enzyme-linked immunosorbent assay, and significantly decreased mRNA levels of MCP-1, as determined using reverse transcription polymerase chain reaction. These results suggest that F. Trogopterori may have therapeutic potential in the control of endothelial disorders caused by inflammation.

Inhibitory effects of antithrombin on the expression of secretory group IIA phospholipase A2 in endothelial cells

  • Kim, Tae-Hoon;Bae, Jong-Sup
    • BMB Reports
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    • v.43 no.9
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    • pp.604-608
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    • 2010
  • Tumor necrosis factor-$\alpha$ (TNF-$\alpha$) mediates proinflammatory responses in primary human umbilical vein endothelial cells (HUVECs), and it upregulates the expression of secretory group IIA phospholipase $A_2$ ($sPLA_2$-IIA). $sPLA_2$-IIA plays a pivotal role in inflammation, and antithrombin (AT) possesses properties that are beneficial to endothelial cells. Therefore, we investigated the effects of AT on the expression of $sPLA_2$-IIA in TNF-$\alpha$-stimulated HUVECs. TNF-$\alpha$ potently upregulated the expression of $sPLA_2$-IIA, and prior treatment of cells with AT inhibited the expression of $sPLA_2$-IIA in HUVECs. Also, antibodies or siRNA for syndecan-4 blocked the protective effect of AT. Furthermore, PI3-kinase and the AKT pathway are significantly involved in the AT-mediated inhibition of the expression of $sPLA_2$-IIA. These results show that AT effectively suppresses the upregulated $sPLA_2$-IIA expression, which might contribute to the cytoprotective effects of AT in the treatment of severe inflammatory diseases.

Inhibitory effect of the extract of Catalpa ovata G. Don. on endothelial adhesion molecule expression (개오동나무 추출물의 내피세포 부착분자 발현 억제 효과)

  • Choi, Byung-Min;Chong, Myong-Soo;Song, Ho-Joon
    • The Korea Journal of Herbology
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    • v.22 no.4
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    • pp.137-143
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    • 2007
  • Objectives : Catalpa ovata G. Don (Bignoniaceae) has been shown to possess a variety of pharmacological activities. However, the effect of Catalpa ovata G. Don on endothelial adhesion molecule expression has not been reported. Methods : To examine the effect of Catalpa ovata G. Don on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), we used various methods such as Western blot analysis, reverse tranascription-polymerase chain reaction (RT-PCR), and luciferase activity assay. Results : 1. The extract of Catalpa ovata G. Don inhibited the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVECs stimulated with TNF-${\alpha}$. 2. The extract of Catalpa ovata G. Don reduced TNF-${\alpha}$-induced adhesion of leukocytes to HUVECs. 3. In addition, The extract of Catalpa ovata G. Don inhibited the promoter activities of ICAM-1 and VCAM-1. Conclusions : These results that Catalpa ovata G. Don may be beneficial in the treatment of inflammatory such as atherosclerosis.

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Free radical scavenging activity of hyangsapyungwisan extract for herbal-acupuncture and protective effects against oxidative damage of HUVECs (향사평위산(香砂平胃散) 약침액(藥鍼液)의 자유기 소거활성 및 혈관내피세포의 산화적 손상에 대한 보호효과)

  • Lim, Sun-Hee;Yi, Hyo-Seung;Moon, Jin-Young
    • Korean Journal of Acupuncture
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    • v.25 no.1
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    • pp.113-130
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    • 2008
  • Objectives : Hyangsapyungwisan (HPS) has been used for treatment of cardiovascular diseases including of arthralgia, myalgia in traditional Korean medicine. However, the medical actions of HPS have not been clearly investigated. The aim of this study was to elucidate the antiradical and antioxidant activity of the extract for herb-acupuncture (HPS-HA) obtained from HPS. Methods & Results : HPS-HA exhibited a stronger inhibition rate (55.5%) on lipid peroxidation of rat liver homogenate induced by $FeCl_2$-ascorbic acid. In addition, HPS-HA markedly interfered with hydroxylradical generation through iron ions chelating action. While pro-oxidant effect of HPS-HA was nearly undetectable at concentrations of 0.5-10㎎/mL. Moerover, HPS-HA revealed a potent antiradical activities on 2,2-diphenyl-1-picryl-hydrazyl (DPPH) radicals, superoxide anions, nitric oxide and peroxynitrite. Furthermore, HPS-HA inhibited copper- and AAPH-mediated oxidation of human low-density lipoprotein (LDL), and also suppressed the relative electrophoretic mobility of LDL. HPS-HA showed strong protective activity against oxidative damage of HUVECs induced by SIN-1. Conclusions : These results suggest that HPS-HA may be effective in protecting against oxidative diseases.

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Thrombin inhibits HMGB1-mediated proinflammatory signaling responses when endothelial protein C receptor is occupied by its natural ligand

  • Bae, Jong-Sup;Rezaie, Alireza R.
    • BMB Reports
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    • v.46 no.11
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    • pp.544-549
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    • 2013
  • High mobility group box 1 (HMGB1) is involved in the pathogenesis of vascular diseases. Unlike activated protein C (APC), the activation of PAR-1 by thrombin is known to elicit proinflammatory responses. To determine whether the occupancy of EPCR by the Gla-domain of APC is responsible for the PAR-1-dependent antiinflammatory activity of the protease, we pretreated HUVECs with the PC zymogen and then activated PAR-1 with thrombin. It was found that thrombin downregulates the HMGB1-mediated induction of both TNF-${\alpha}$ and IL-6 and inhibits the activation of both p38 MAPK and NF-${\kappa}B$ in HUVECs pretreated with PC. Furthermore, thrombin inhibited HMGB1-mediated hyperpermeability and leukocyte adhesion/migration by inhibiting the expression of cell adhesion molecules in HUVECs if EPCR was occupied. Collectively, these results suggest the concept that thrombin can initiate proinflammatory responses in vascular endothelial cells through the activation of PAR-1 may not hold true for normal vessels expressing EPCR under in vivo conditions.

Korean Red Ginseng water extract inhibits COX-2 expression by suppressing p38 in acrolein-treated human endothelial cells

  • Lee, Seung Eun;Park, Yong Seek
    • Journal of Ginseng Research
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    • v.38 no.1
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    • pp.34-39
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    • 2014
  • Cigarette smoke is considered a major risk factor for vascular diseases. There are many toxic compounds in cigarette smoke, including acrolein and other ${\alpha},{\beta}$-unsaturated aldehydes, which are regarded as mediators of inflammation and vascular dysfunction. Furthermore, recent studies have revealed that acrolein, an ${\alpha},{\beta}$-unsaturated aldehyde in cigarette smoke, induces inflammatory mediator expression, which is known to be related to vascular diseases. In this study, we investigated whether Korean Red Ginseng (KRG) water extract suppressed acrolein-induced cyclooxygenase (COX)-2 expression in human umbilical vein endothelial cells (HUVECs). Acrolein-induced COX-2 expression was accompanied by increased levels of phosphorylated p38 in HUVECs and KRG inhibited COX-2 expression in HUVECs. These results suggest that KRG suppresses acrolein-induced COX-2 expression via inhibition of the p38 mitogen-activated protein kinase signaling pathway. In addition, KRG exhibited an inhibitory effect on acrolein-induced apoptosis, as demonstrated by annexin Vepropidium iodide staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay. Consistent with these results, KRG may exert a vasculoprotective effect through inhibition of COX-2 expression in acrolein-stimulated human endothelial cells.