Document Detail

Catalpol inhibits apoptosis in hydrogen peroxide-induced endothelium by activating the PI3K/Akt signaling pathway and modulating expression of Bcl-2 and Bax.
MedLine Citation:
PMID:  19962976     Owner:  NLM     Status:  MEDLINE    
Catalpol, an iridoid glucoside found in the root of Rehmannia glutinosa Libosch, has been demonstrated to reduce apoptosis in neuronal cell lines. Recent data suggests that catalpol also exerts anti-apoptotic effects on other cell types. The aim of the present study was to investigate whether catalpol protects against hydrogen peroxide (H(2)O(2)) induced apoptosis in human umbilical vein endothelial cells (HUVECs). Apoptotic cells were detected by terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling, Annexin V-fluorescein isothiocyanate binding assay and by assessment of caspase-3 activity. The level of intracellular reactive oxygen species was quantified by 2', 7'-dichlorofluorescein diacetate assay. Expression of Akt, Bad, Bcl-2 and Bax mRNA and protein was determined by real-time semiquantitative reverse transcription-polymerase chain reaction and Western blotting. Apoptosis in HUVECs was associated with increased Bax, decreased Bcl-2 activity and inactivated phosphorylation of Akt and Bad after 24h of H(2)O(2) exposure. Pre-treatment of HUVECs with catalpol significantly reduced H(2)O(2)-induced intracellular reactive oxygen species release. Catalpol not only increased the expression of Bcl-2, while decreasing Bax expression, but also induced Akt activation and Bad phosphorylation, and ultimately reduced H(2)O(2)-induced apoptosis. The protective effects of catalpol were partially inhibited by the phosphatidylinositol 3-kinase (PI3K) antagonist wortmannin or 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002). Taken together, these results suggest that pre-treatment of HUVECs with catalpol can block H(2)O(2)-induced apoptosis, and that the underlying mechanism involves reactive oxygen species scavenging, activation of the PI3K/Akt-Bad signaling pathway and increased Bcl-2 and decreased Bax expression.
Lingai Hu; Yukun Sun; Jian Hu
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Publication Detail:
Type:  Journal Article     Date:  2009-12-03
Journal Detail:
Title:  European journal of pharmacology     Volume:  628     ISSN:  1879-0712     ISO Abbreviation:  Eur. J. Pharmacol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-27     Completed Date:  2010-04-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1254354     Medline TA:  Eur J Pharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  155-63     Citation Subset:  IM    
Department of Cardiology, The First Affiliated Hospital of China Medical University, Liaoning, China.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / metabolism
Apoptosis / drug effects*
Cell Survival / drug effects
Endothelial Cells / cytology,  drug effects,  metabolism
Endothelium, Vascular / cytology,  drug effects*,  metabolism
Free Radical Scavengers / pharmacology*
Gene Expression Regulation / drug effects*
Hydrogen Peroxide / pharmacology*
Phosphorylation / drug effects
Proto-Oncogene Proteins c-akt / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
Quaternary Ammonium Compounds / pharmacology*
Reactive Oxygen Species / metabolism
Signal Transduction / drug effects*
Umbilical Veins / cytology
bcl-2-Associated X Protein / metabolism
Reg. No./Substance:
0/Free Radical Scavengers; 0/Proto-Oncogene Proteins c-bcl-2; 0/Quaternary Ammonium Compounds; 0/Reactive Oxygen Species; 0/bcl-2-Associated X Protein; 64365-16-8/catamine AB; 7722-84-1/Hydrogen Peroxide; EC 3-Kinase; EC Proteins c-akt

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