作者: Rai Ajit K. Srivastava
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摘要: Estrogens are suggested to be antiatherogenic by affecting the vessel wall components. Since ABCA1 was recently shown atheroprotective, it examined if estrogen-induced atheroprotection occurs partly via regulation of ABCA1. hepatic expression also contribute bulk HDL levels, under conditions high or low levels were investigated in mice expressing normal elevated apoAI. To delineate whether estrogen’s effect estrogen receptor-α-mediated pathway, receptor-α-deficient (ER-α) –/– administered either placebo β-estradiol for 5 consecutive days. Estrogen treatments decreased circulating 30%, but increased and intestinal mRNA 2- 1.5-fold, respectively. Hepatic ER-α 3-fold. These results suggest that estrogen, despite lowering HDL, up-regulated mRNA, absence ER-α, ER-β could compensate ER-α. study correlate with expression, wild-type (WT) apoAI transgenic (A1-Tg) fed fat (HF) diet without cholic acid (CA) 3 weeks. One group treated fenofibrate, known elevate levels. CA HF while fenofibrate However, neither nor altered 1.8-fold WT, lowered 2-fold A1-Tg mice, suggesting did not basal influenced expression. data show first time effects may occur ABCA1mediated influence (Mol Cell Biochem 240: 67–73, 2002)