| Epigallocatechin-3-gallate ameliorates hyperglycemia-induced embryonic vasculopathy and malformation by inhibition of Foxo3a activation. | |
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MedLine Citation:
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PMID: 20417490 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Peixin Yang; Hua Li |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural Date: 2010-04-24 |
Journal Detail:
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Title: American journal of obstetrics and gynecology Volume: 203 ISSN: 1097-6868 ISO Abbreviation: Am. J. Obstet. Gynecol. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-08 Completed Date: 2010-09-03 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 0370476 Medline TA: Am J Obstet Gynecol Country: United States |
Other Details:
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Languages: eng Pagination: 75.e1-6 Citation Subset: AIM; IM |
Copyright Information:
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Copyright (c) 2010 Mosby, Inc. All rights reserved. |
Affiliation:
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Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants / pharmacology* Blotting, Western Catechin / analogs & derivatives*, pharmacology Disease Models, Animal Embryonic Development / drug effects* Female Fetus Forkhead Transcription Factors / antagonists & inhibitors*, metabolism Hyperglycemia / drug therapy*, enzymology Oxidative Stress / drug effects* Phosphorylation / drug effects Pregnancy Proto-Oncogene Proteins c-akt / antagonists & inhibitors, metabolism Rats Rats, Sprague-Dawley Signal Transduction Yolk Sac / anatomy & histology, blood supply |
| Grant Support | |
ID/Acronym/Agency:
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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 |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Forkhead Transcription Factors; 0/Foxo3a protein, rat; 154-23-4/Catechin; 989-51-5/epigallocatechin gallate; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
| Comments/Corrections | |
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