Document Detail


The ginsenoside protopanaxatriol protects endothelial cells from hydrogen peroxide-induced cell injury and cell death by modulating intracellular redox status.
MedLine Citation:
PMID:  19932166     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ginsenosides, the active components of the famous Chinese herb ginseng, have been suggested to possess cardiovascular-protective effects. The mechanism of ginsenosides is believed to be associated with their ability to prevent cellular oxidative stress. The purpose of this study was to explore the cytoprotective effects of the ginsenoside protopanaxatriol (PPT) on hydrogen peroxide (H(2)O(2))-induced endothelial cell injury and cell death. Pretreatment of human umbilical vein endothelial cells (HUVECs) with PPT for 24 h was able to protect the cells against H(2)O(2)-induced injury. In addition to cell death, pretreatment with PPT could also reduce H(2)O(2)-induced DNA damage, overactivation of the DNA repair enzyme PARP-1, and concomitant depletion of the intracellular substrate NAD(+). Furthermore, PPT could reverse the decrease in ATP/ADP ratio caused by H(2)O(2). The metabolism of glutathione was also changed. H(2)O(2) could induce a significant decrease in GSH level resulting in a decrease in the GSH/GSSG ratio. This could be prevented by pretreatment with PPT. The action was associated with increasing activities of the GSH-metabolizing enzymes glutathione reductase and glutathione peroxidase. These findings suggest that the ginsenoside PPT could protect HUVECs against H(2)O(2)-induced cell death via its action against oxidative stress, which may be responsible for the cardiovascular-protective action of ginseng.
Authors:
Hoi Hin Kwok; Wai Yee Ng; Mildred Sze Ming Yang; Nai Ki Mak; Ricky Ngok Shun Wong; Patrick Ying Kit Yue
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-11-20
Journal Detail:
Title:  Free radical biology & medicine     Volume:  48     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-03     Completed Date:  2010-04-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  437-45     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Elsevier Inc. All rights reserved.
Affiliation:
Department of Biology, Faculty of Science, Hong Kong Baptist University, Kowloon Tong, Hong Kong SAR, China.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Cells, Cultured
Endothelium, Vascular / cytology,  drug effects*,  metabolism
Ginsenosides / pharmacology*
Glutathione / metabolism
Glutathione Disulfide / metabolism
Glutathione Peroxidase / metabolism
Glutathione Reductase / metabolism
Humans
Hydrogen Peroxide / pharmacology*
L-Lactate Dehydrogenase / metabolism
NAD / metabolism
Oxidants / pharmacology*
Oxidation-Reduction
Oxidative Stress
Panax / chemistry
Poly(ADP-ribose) Polymerases / metabolism
Sapogenins / pharmacology*
Umbilical Veins / cytology,  drug effects,  metabolism
Chemical
Reg. No./Substance:
0/Ginsenosides; 0/Oxidants; 0/Sapogenins; 27025-41-8/Glutathione Disulfide; 34080-08-5/protopanaxatriol; 53-84-9/NAD; 70-18-8/Glutathione; 7722-84-1/Hydrogen Peroxide; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.8.1.7/Glutathione Reductase; EC 2.4.2.30/Poly(ADP-ribose) Polymerases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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