期刊
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
卷 203, 期 1, 页码 -出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2010.02.008
关键词
Akt activation; epigallocatechin-3-gallate; Foxo3a activation; hyperglycemia; malformations; vasculopathy
资金
- National Institutes of Health [R01 DK083243, K12HD043489]
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 mu mol/L of EGCG. RESULTS: Both 1 and 10 mu mol/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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