• Title/Summary/Keyword: Catalpa ovata G. Don

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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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Isolation and identification of lignans as Antioxidant from loaves of Catalpa ovata G. $D_{ON}$ (개오동나무 잎으로부터 항산화 활성을 갖는 lignan 화합물의 분리 및 동정)

  • 국주희;마승진;문제학;박근형
    • KSBB Journal
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    • v.18 no.6
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    • pp.511-516
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    • 2003
  • The methanol extract from leaves of Catalpa ovata 6. DoN showed DPPH (1,1-diphenyl-2-picrylhydrazyl) radical-scavenging activity, and its antioxidative compounds were studied. The ethyl acetate-soluble neutral fraction from the methanol extract was successively purified with silica gel adsorption column chromatography, Sephadex LH-20 column chromatography and HPLC. Three antioxidative compounds were isolated and identified as piperitol, pinoresinol and lariciresinol by HR-MS and NMR spectroscopic analyses. The DPPH radical-scavenging activity of the identified compounds decreased in the order of lariciresinol > pinoresinol > piperitol.

Studies on the Anti-inflammatory and Anti-apoptotic Effect of Catalposide Isolated from Catalpa ovata (개오동나무에서 추출(抽出)한 Catalposide의 항염(抗炎) 및 세포고사(細胞枯死) 억제효과(抑制效果)에 관(關)한 연구(硏究))

  • Oh, Cheon-Sik;Hwang, Sang-Wook;Kim, Yong-Woo;Song, Dal-Soo;Chae, Young-Seok;Jeong, Jong-Gil;Song, Ho-Joon;Shin, Min-Kyo
    • The Korea Journal of Herbology
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    • v.20 no.3
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    • pp.29-41
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    • 2005
  • Objectives : The use of natural products with therapeutic properties is as ancient as human civilisation and, for a long time, mineral, plant and animal products were the main sources of drugs. Catalposide, the major iridoid glycoside isolated from the stem bark of Catalpa ovata G. Don (Bignoniceae) has been shown to possess anti-microbial and anti-tumoral properties. Heme oxygenase-1 (HO-1) is a stress response protein and is known to play a protective role against the oxidative injury. In this study, we examined whether catalposide could protect Neuro 2A cells, a kind of neuronal cell lines, from oxidative damage through the induction of HO-1 protein expression and HO activity. We also examined the effects of catalposide on the productions of tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ and nitric oxide (NO) on RAW 264.7 macrophages activated with the endotoxin lipopolysaccharide. Methods : HO-1 expression in Neuro 2A cells was measured by Western blotting analysis. NO and $TNF--{\alpha}$ produced by RAW 264.7 macrophage were measured by Griess reagent and enzyme-linked immunosorbent assay, respectively. Results : The treatment of the cells with catalposide resulted in dose- and time-dependent up-regulations of both HO-1 protein expression and HO activity. Catalposide protected the cells from hydrogen peroxide-induced cell death. The protective effect of catalposide on hydrogen peroxide-induced cell death was abrogated by zinc protoporphyrin IX, a HO inhibitor. Additional experiments revealed the involvement of CO in the cytoprotective effect of catalposide-induced HO-1. In addition, catalposide inhibited the productions of $TNF--{\alpha}$ and NO with significant decreases in mRNA levels of $TNF--{\alpha}$ and inducible NO synthase. Conclusions : Our results indicate that catalposide is a potent inducer of HO-1 and HO-1 induction is responsible for the catalposide-mediated cytoprotection against oxidative damage and that catalposide may have therapeutic potential in the control of inflammatory disorders.

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