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Cytoprotection of human endothelial cells against oxidative stress by 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im): Application of systems biology to understand the mechanism of action

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2014.03.033 Byline: Xinyu Wang, James A. Bynum, Solomon Stavchansky, Phillip D. Bowman Abstract: Cellular damage from oxidative stress, in particular following ischemic injury, occurs during heart attac... Full description

Journal Title: European Journal of Pharmacology July 5, 2014, Vol.734, p.122(10)
Main Author: Wang, Xinyu
Other Authors: Bynum, James A. , Stavchansky, Solomon , Bowman, Phillip D.
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Cengage Learning, Inc.
ID: ISSN: 0014-2999
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recordid: gale_ofa369540855
title: Cytoprotection of human endothelial cells against oxidative stress by 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im): Application of systems biology to understand the mechanism of action
format: Article
creator:
  • Wang, Xinyu
  • Bynum, James A.
  • Stavchansky, Solomon
  • Bowman, Phillip D.
subjects:
  • Heat Shock Proteins
  • Biological Products
  • Oxidative Stress
  • Enzymes
  • Nitriles
  • Gene Expression
  • Drugstores
  • Endothelium
ispartof: European Journal of Pharmacology, July 5, 2014, Vol.734, p.122(10)
description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2014.03.033 Byline: Xinyu Wang, James A. Bynum, Solomon Stavchansky, Phillip D. Bowman Abstract: Cellular damage from oxidative stress, in particular following ischemic injury, occurs during heart attack, stroke, or traumatic injury, and is potentially reducible with appropriate drug treatment. We previously reported that caffeic acid phenethyl ester (CAPE), a plant-derived polyphenolic compound, protected human umbilical vein endothelial cells (HUVEC) from menadione-induced oxidative stress and that this cytoprotective effect was correlated with the capacity to induce heme oxygenase-1 (HMOX1) and its protein product, a phase II cytoprotective enzyme. To further improve this cytoprotective effect, we studied a synthetic triterpenoid, 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im), which is known as a potent phase II enzyme inducer with antitumor and anti-inflammatory activities, and compared it to CAPE. CDDO-Im at 200nM provided more protection to HUVEC against oxidative stress than 20[mu]M CAPE. We explored the mechanism of CDDO-Im cytoprotection with gene expression profiling and pathway analysis and compared to that of CAPE. In addition to potent up-regulation of HMOX1, heat shock proteins (HSP) were also found to be highly induced by CDDO-Im in HUVEC. Pathway analysis results showed that transcription factor Nrf2-mediated oxidative stress response was among the top canonical pathways commonly activated by both CDDO-Im and CAPE. Compared to CAPE, CDDO-Im up-regulated more HSP and some of them to a much higher extent. In addition, CDDO-Im treatment affected Nrf2 pathway more significantly. These findings may provide an explanation why CDDO-Im is a more potent cytoprotectant than CAPE against oxidative stress in HUVEC. Author Affiliation: (a) Department of Pharmaceutical Sciences, School of Pharmacy, Philadelphia College of Osteopathic Medicine-Georgia Campus, 625 Old Peachtree Road NW, Suwanee, GA 30024-2937, USA (b) US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, USA (c) Division of Pharmaceutics, College of Pharmacy, University of Texas at Austin, TX 77812, USA Article History: Received 13 December 2013; Revised 18 March 2014; Accepted 24 March 2014
language: English
source: Cengage Learning, Inc.
identifier: ISSN: 0014-2999
fulltext: fulltext
issn:
  • 0014-2999
  • 00142999
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titleCytoprotection of human endothelial cells against oxidative stress by 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im): Application of systems biology to understand the mechanism of action
creatorWang, Xinyu ; Bynum, James A. ; Stavchansky, Solomon ; Bowman, Phillip D.
ispartofEuropean Journal of Pharmacology, July 5, 2014, Vol.734, p.122(10)
identifierISSN: 0014-2999
subjectHeat Shock Proteins ; Biological Products ; Oxidative Stress ; Enzymes ; Nitriles ; Gene Expression ; Drugstores ; Endothelium
descriptionTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2014.03.033 Byline: Xinyu Wang, James A. Bynum, Solomon Stavchansky, Phillip D. Bowman Abstract: Cellular damage from oxidative stress, in particular following ischemic injury, occurs during heart attack, stroke, or traumatic injury, and is potentially reducible with appropriate drug treatment. We previously reported that caffeic acid phenethyl ester (CAPE), a plant-derived polyphenolic compound, protected human umbilical vein endothelial cells (HUVEC) from menadione-induced oxidative stress and that this cytoprotective effect was correlated with the capacity to induce heme oxygenase-1 (HMOX1) and its protein product, a phase II cytoprotective enzyme. To further improve this cytoprotective effect, we studied a synthetic triterpenoid, 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im), which is known as a potent phase II enzyme inducer with antitumor and anti-inflammatory activities, and compared it to CAPE. CDDO-Im at 200nM provided more protection to HUVEC against oxidative stress than 20[mu]M CAPE. We explored the mechanism of CDDO-Im cytoprotection with gene expression profiling and pathway analysis and compared to that of CAPE. In addition to potent up-regulation of HMOX1, heat shock proteins (HSP) were also found to be highly induced by CDDO-Im in HUVEC. Pathway analysis results showed that transcription factor Nrf2-mediated oxidative stress response was among the top canonical pathways commonly activated by both CDDO-Im and CAPE. Compared to CAPE, CDDO-Im up-regulated more HSP and some of them to a much higher extent. In addition, CDDO-Im treatment affected Nrf2 pathway more significantly. These findings may provide an explanation why CDDO-Im is a more potent cytoprotectant than CAPE against oxidative stress in HUVEC. Author Affiliation: (a) Department of Pharmaceutical Sciences, School of Pharmacy, Philadelphia College of Osteopathic Medicine-Georgia Campus, 625 Old Peachtree Road NW, Suwanee, GA 30024-2937, USA (b) US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, USA (c) Division of Pharmaceutics, College of Pharmacy, University of Texas at Austin, TX 77812, USA Article History: Received 13 December 2013; Revised 18 March 2014; Accepted 24 March 2014
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titleCytoprotection of human endothelial cells against oxidative stress by 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im): Application of systems biology to understand the mechanism of action.
descriptionTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2014.03.033 Byline: Xinyu Wang, James A. Bynum, Solomon Stavchansky, Phillip D. Bowman Abstract: Cellular damage from oxidative stress, in particular following ischemic injury, occurs during heart attack, stroke, or traumatic injury, and is potentially reducible with appropriate drug treatment. We previously reported that caffeic acid phenethyl ester (CAPE), a plant-derived polyphenolic compound, protected human umbilical vein endothelial cells (HUVEC) from menadione-induced oxidative stress and that this cytoprotective effect was correlated with the capacity to induce heme oxygenase-1 (HMOX1) and its protein product, a phase II cytoprotective enzyme. To further improve this cytoprotective effect, we studied a synthetic triterpenoid, 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im), which is known as a potent phase II enzyme inducer with antitumor and anti-inflammatory activities, and compared it to CAPE. CDDO-Im at 200nM provided more protection to HUVEC against oxidative stress than 20[mu]M CAPE. We explored the mechanism of CDDO-Im cytoprotection with gene expression profiling and pathway analysis and compared to that of CAPE. In addition to potent up-regulation of HMOX1, heat shock proteins (HSP) were also found to be highly induced by CDDO-Im in HUVEC. Pathway analysis results showed that transcription factor Nrf2-mediated oxidative stress response was among the top canonical pathways commonly activated by both CDDO-Im and CAPE. Compared to CAPE, CDDO-Im up-regulated more HSP and some of them to a much higher extent. In addition, CDDO-Im treatment affected Nrf2 pathway more significantly. These findings may provide an explanation why CDDO-Im is a more potent cytoprotectant than CAPE against oxidative stress in HUVEC. Author Affiliation: (a) Department of Pharmaceutical Sciences, School of Pharmacy, Philadelphia College of Osteopathic Medicine-Georgia Campus, 625 Old Peachtree Road NW, Suwanee, GA 30024-2937, USA (b) US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, USA (c) Division of Pharmaceutics, College of Pharmacy, University of Texas at Austin, TX 77812, USA Article History: Received 13 December 2013; Revised 18 March 2014; Accepted 24 March 2014
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abstractTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2014.03.033 Byline: Xinyu Wang, James A. Bynum, Solomon Stavchansky, Phillip D. Bowman Abstract: Cellular damage from oxidative stress, in particular following ischemic injury, occurs during heart attack, stroke, or traumatic injury, and is potentially reducible with appropriate drug treatment. We previously reported that caffeic acid phenethyl ester (CAPE), a plant-derived polyphenolic compound, protected human umbilical vein endothelial cells (HUVEC) from menadione-induced oxidative stress and that this cytoprotective effect was correlated with the capacity to induce heme oxygenase-1 (HMOX1) and its protein product, a phase II cytoprotective enzyme. To further improve this cytoprotective effect, we studied a synthetic triterpenoid, 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im), which is known as a potent phase II enzyme inducer with antitumor and anti-inflammatory activities, and compared it to CAPE. CDDO-Im at 200nM provided more protection to HUVEC against oxidative stress than 20[mu]M CAPE. We explored the mechanism of CDDO-Im cytoprotection with gene expression profiling and pathway analysis and compared to that of CAPE. In addition to potent up-regulation of HMOX1, heat shock proteins (HSP) were also found to be highly induced by CDDO-Im in HUVEC. Pathway analysis results showed that transcription factor Nrf2-mediated oxidative stress response was among the top canonical pathways commonly activated by both CDDO-Im and CAPE. Compared to CAPE, CDDO-Im up-regulated more HSP and some of them to a much higher extent. In addition, CDDO-Im treatment affected Nrf2 pathway more significantly. These findings may provide an explanation why CDDO-Im is a more potent cytoprotectant than CAPE against oxidative stress in HUVEC. Author Affiliation: (a) Department of Pharmaceutical Sciences, School of Pharmacy, Philadelphia College of Osteopathic Medicine-Georgia Campus, 625 Old Peachtree Road NW, Suwanee, GA 30024-2937, USA (b) US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, USA (c) Division of Pharmaceutics, College of Pharmacy, University of Texas at Austin, TX 77812, USA Article History: Received 13 December 2013; Revised 18 March 2014; Accepted 24 March 2014
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