Document Detail

Epigallocatechin-3-gallate ameliorates hyperglycemia-induced embryonic vasculopathy and malformation by inhibition of Foxo3a activation.
MedLine Citation:
PMID:  20417490     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Maternal hyperglycemia increases the risk of congenital malformations. Epigallocatechin-3-gallate (EGCG), a natural antioxidant purified from green tea, inhibits oxidative stress signaling. We propose that EGCG prevents hyperglycemia-induced malformation via inhibition of oxidative stress signaling. The objective of this study is to examine the effect of EGCG on hyperglycemia-induced adverse effects during embryonic development.
STUDY DESIGN: Day-9 rat conceptuses were cultured under euglycemic (150 mg/dL glucose) and hyperglycemic (300 mg/dL glucose) conditions in the presence or absence of 1 or 10 micromol/L of EGCG.
RESULTS: Both 1 and 10 micromol/L of EGCG significantly ameliorated hyperglycemia-induced embryonic vasculopathy and malformations. Hyperglycemia inactivated protein kinase B (Akt) by reducing phosphorylated Akt levels. EGCG reversed the inhibitory effect of hyperglycemia on Akt activation. EGCG also prevented hyperglycemia-reduced phosphorylated Forkhead transcription factor 3a levels.
CONCLUSION: EGCG prevented hyperglycemia-induced embryopathy through inhibition of Forkhead transcription factor 3a activation. This may have been mediated via the activation of Akt. These findings offer the potential for a possible pharmacological prophylaxis for hyperglycemia-induced embryonic malformations.
Peixin Yang; Hua Li
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural     Date:  2010-04-24
Journal Detail:
Title:  American journal of obstetrics and gynecology     Volume:  203     ISSN:  1097-6868     ISO Abbreviation:  Am. J. Obstet. Gynecol.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-08     Completed Date:  2010-09-03     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  0370476     Medline TA:  Am J Obstet Gynecol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  75.e1-6     Citation Subset:  AIM; IM    
Copyright Information:
Copyright (c) 2010 Mosby, Inc. All rights reserved.
Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antioxidants / pharmacology*
Blotting, Western
Catechin / analogs & derivatives*,  pharmacology
Disease Models, Animal
Embryonic Development / drug effects*
Forkhead Transcription Factors / antagonists & inhibitors*,  metabolism
Hyperglycemia / drug therapy*,  enzymology
Oxidative Stress / drug effects*
Phosphorylation / drug effects
Proto-Oncogene Proteins c-akt / antagonists & inhibitors,  metabolism
Rats, Sprague-Dawley
Signal Transduction
Yolk Sac / anatomy & histology,  blood supply
Grant Support
K12 HD043489/HD/NICHD NIH HHS; K12 HD043489-08/HD/NICHD NIH HHS; R01 DK083243/DK/NIDDK NIH HHS; R01 DK083243-01A2/DK/NIDDK NIH HHS
Reg. No./Substance:
0/Antioxidants; 0/Forkhead Transcription Factors; 0/Foxo3a protein, rat; 154-23-4/Catechin; BQM438CTEL/epigallocatechin gallate; EC Proteins c-akt

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

Previous Document:  Clinical outcome in neonates with twin anemia-polycythemia sequence.
Next Document:  Care for women with prior preterm birth.