• Title/Summary/Keyword: ICAM

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The Effect of Acanthopanax sessiliflorum Cheonghyeol Plus on NF-κB and MAPKs Signaling and Vascular Attachment Factors (오가피청혈플러스가 NF-κB 및 MAPKs 신호전달체계와 혈관부착인자 등에 미치는 영향)

  • Lee, Ji-won;Choi, Gyu-cheol;Bae, Ji-eun;Yoo, Ho-ryong;Kim, Yoon-sik;Seol, In-chan
    • The Journal of Internal Korean Medicine
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    • v.41 no.6
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    • pp.967-983
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    • 2020
  • Objective: This study was performed to investigate the effect of Acanthopanax sessiliflorum Cheonghyeol plus (ASCP) on NF-κB and MAPK signaling and vascular adhesion factors associated with dyslipidemia in human umbilical vein endothelial cells (HUVECs). Methods: We measured the scavenging activity of DPPH radical and ABTS radical by ASCP in HUVECs. We measured the protein expression levels of NF-κB, IκBα, ERK, JNK, and p38 after treatment of HUVECs with TNF-α. We measured the expression levels of MCP-1, ICAM-1, and VCAM-1 mRNA and of MCP-1, ICAM-1, and VCAM-1 biomarkers after treatment of HUVECs with TNF-α. Results: The DPPH and ABTS radical scavenging activity of ASCP increased in a concentration-dependent manner. NF-κB, IκB, ERK, p38 protein expression levels decreased following ASCP treatment at all concentrations compared to untreated control HUVECs. JNK protein expression levels decreased in ASCP-treated HUVECs compared to untreated controls at concentrations of 100 ㎍/mL. MCP-1 mRNA expression level decreased with ASCP treatment ≥200 ㎍/mL compared to the control. ICAM-1 and VCAM-1 mRNA expression levels decreased at all concentrations compared to the control. MCP-1 protein expression level was reduced compared to the control at concentrations ≥200 ㎍/mL, ICAM-1 protein expression level was reduced compared to the control at concentrations ≥100 ㎍/mL, and VCAM-1 protein expression level was reduced at all concentrations. Conclusions: These results suggest that ASCP has an antioxidative and hypolipidemic effect and that ASCP could treat and prevent dyslipidemia, atherosclerosis, and cardio-cerebrovascular 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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The Protective Effect of Prostaglandin E1 Against Ischemia-reperfusion Injury of Musculocutaneous Flaps (백서 복직근피판에 있어 허혈-재혈류 손상에 미치는 Prostaglandin E1의 예방효과)

  • Hong, Joon Pio;Chung, Yoon Kyu;Chung, Soon-Hee
    • Archives of Reconstructive Microsurgery
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    • v.9 no.2
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    • pp.190-198
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    • 2000
  • 본 연구는 백서 복직근피판에 있어 허혈-재혈류 손상에 미치는 prostaglandin E1(PGE-1)의 예방효과를 분석 실험하였으며, 그 기전으로 내피세포의 intercellular adhesion molecule-1(ICAM-1)이 down regulation 됨을 확인하였다. 기존의 PGE-1은 혈관 확장 및 혈소판 응고 저하 등의 기전으로 피판 이식술 후 주로 사용하였으나, 허혈-재혈류 손상 시에 PGE-1 역할에 대한 연구는 잘 알려진바 없다. 허혈-재혈류 손상에 대한 기전은 현재 여러 가설로 설명되고 있으나, 최근 내피 세포와 백혈구의 역할이 주목을 받고 있다. 장시간 허혈 상태의 피판은 재혈류시 백혈구가 내피세포에 접착함으로써 직간접적인 경로로 독소를 생성하며, 결국 내피세포 및 주변조직의 괴사로 이어진다. 본 연구는 면역조직학 염색을 통한 내피세포의 ICAM-1 발현 억제와 그로 인한 백혈구의 내피세포 접착 억제를 그 기전으로 볼 수 있었으며, PGE-1을 술 중 투여함으로써 피판의 생존율을 향상시킬 수 있었다.

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A Role of Mitogen Activated Protein Kinases and Inflammatory Responses in Gender Differences in Kidney Ischemia Injury

  • Park, Kwon-Moo;Han, Ho-Jae
    • The Korean Journal of Physiology and Pharmacology
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    • v.6 no.3
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    • pp.155-160
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    • 2002
  • It is not known whether gender differences play a role in susceptibility to ischemic acute renal failure. Thus, we examined if there were any differences in susceptibility between male and female mice to kidney ischemic injury, and if so, whether it is due to differences in mitogen activated protein kinases (MAPKs) or inflammatory responses to ischemia. Female mice were protected against kidney ischemia when compared with males. Thirty minutes of bilateral ischemia resulted in marked functional and morphological damages in males, but not in females. The ischemia-induced phosphorylation of c-jun N-terminal stress-activated protein kinases (JNKs) was higher in males than in females. Phosphorylation of extracellular signal-regulated kinases (ERKs) was lower in males than in females. Post- ischemia medullary infiltration of RAW 264.7 cell, a monocyte-macrophage cell, and intercellular adhesion molecule-1 (ICAM-1) were greater in males than in females. In conclusion, males were much more susceptible to ischemia than females. The enhanced propensity to ischemic injury in males was correlated with greater activation of JNKs, greater expression of ICAM-1, and greater trapping of leukocytes in the medulla.

Butein, a tetrahydroxychalcone, suppresses pro-inflammatory responses in HaCaT keratinocytes

  • Seo, Won Yong;Youn, Gi Soo;Choi, Soo Young;Park, Jinseu
    • BMB Reports
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    • v.48 no.9
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    • pp.495-500
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    • 2015
  • Up-regulation of cell adhesion molecules and proinflammatory cytokines contributes to enhanced monocyte adhesiveness and infiltration into the skin, during the pathogenesis of various inflammatory skin diseases, including atopic dermatitis. In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes. Butein significantly inhibited TNF-α-induced ICAM-I expression and monocyte adhesion in human keratinocyte cell line HaCaT. Butein also decreased TNF-α-induced pro-inflammatory mediators, such as IL-6, IP-10 and MCP-1, in HaCaT cells. Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells. In addition, treatment of HaCaT cells with butein suppressed TNF-α-induced MAPK activation. Furthermore, butein suppressed TNF-α-induced NF-kappaB activation. Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of proinflammatory mediators in keratinocytes. Therefore, butein may be used as a therapeutic agent for the treatment of inflammatory skin diseases. [BMB Reports 2015; 48(9): 495-500]

Inhibition of $\gamma$-Irradiation Induced Adhesion Molecules and NO Production by Alginate in Human Endothelial Cells

  • Son, Eun-Wha;Cho, Chul-Koo;Rhee, Dong-Kwon;Pyo, Suhk-Neung
    • Archives of Pharmacal Research
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    • v.24 no.5
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    • pp.466-471
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    • 2001
  • 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 (VCAM-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, interioring with the expression of adhesion molecules is an important therapeutic target. In the present study, we demonstrate that high mannronic acid-containing alginate (HMA) inhibits $\gamma$IR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose dependent manner. HMA also inhibited $\gamma$IR induced production of Nitric oxide (NO). These data suggest that HMA has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.

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