Genistein, daidzein and glycitein inhibit growth and DNA synthesis of aortic smooth muscle cells from stroke-prone spontaneously hypertensive rats

Citation
W. Pan et al., Genistein, daidzein and glycitein inhibit growth and DNA synthesis of aortic smooth muscle cells from stroke-prone spontaneously hypertensive rats, J NUTR, 131(4), 2001, pp. 1154-1158
Citations number
37
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
0022-3166 → ACNP
Volume
131
Issue
4
Year of publication
2001
Pages
1154 - 1158
Database
ISI
SICI code
0022-3166(200104)131:4<1154:GDAGIG>2.0.ZU;2-1
Abstract
Recent studies have reported that estrogen replacement therapy (ERT) reduce s the risk of cardiovascular diseases in postmenopausal women. However, mec hanisms responsible for this effect are not yet completely understood, and ERT is associated with carcinogenic side effects in women and feminizing ef fects in men. Because soybean isoflavones, a group of natural phytoestrogen s, have only weak estrogenic activity and are not known to have side effect s such as carcinogenesis and feminization, we evaluated the effects of geni stein, daidzein and glycitein on the growth and DNA synthesis of aortic smo oth muscle cells (SMC) from stroke-prone spontaneously hypertensive rats (S HRSP). SMC were cultured in dishes and proliferated on 10% dextran-coated c harcoal/fetal bovine serum, and then treated with 0.1-30 mu mol/L of genist ein, daidzein or glycitein to investigate cell proliferation (cell number) and DNA synthesis (cell proliferation ELISA system), respectively. We also studied their effects on platelet-derived growth factor (PDGF)-BB (20 mug/L )-induced SMC proliferation. Soybean isoflavones inhibited proliferation an d DNA synthesis of SMC from SHRSP in a concentration-dependent manner. Inhi bition was significant at 3 mu mol/L of genistein and 10 mu mol/L of both d aidzein and glycitein. For significant inhibition of PDGF-BB-induced SMC pr oliferation, concentrations as low as 0.1 mu mol/L of each isoflavone were effective. These isoflavones, with their inhibitory effects on natural and PDGF-BB-induced SMC proliferation, may be useful in attenuatating such prol iferation, a basic mechanism involved in atherosclerotic vascular change, t hereby preventing atherosclerotic cardiovascular diseases.