title: Genistein attenuates vascular endothelial impairment in ovariectomized hyperhomocysteinemic rats.
abstract: Hyperhomocysteinemia (HHcy) is a well-known independent risk factor for vascular diseases in the general population. This study was to explore the effect of genistein (GST), a natural bioactive compound derived from legumes, on HHcy-induced vascular endothelial impairment in ovariectomized rats in vivo. Thirty-two adult female Wistar rats were assigned randomly into four groups (n = 8): (a) Con: control; (b) Met: 2.5% methionine diet; (c) OVX + Met: ovariectomy + 2.5% methionine diet; (d) OVX + Met + GST: ovariectomy + 2.5% methionine diet + supplementation with genistein. After 12 wk of different treatment, the rats' blood, toracic aortas and liver samples were collected for analysis. Results showed that high-methionine diet induced both elevation of plasma Hcy and endothelial dysfunction, and ovariectomy deteriorated these injuries. Significant improvement of both functional and morphological changes of vascular endothelium was observed in OVX + Met + GST group; meanwhile the plasma Hcy levels decreased remarkably. There were significant elevations of plasma ET-1 and liver MDA levels in ovariectomized HHcy rats, and supplementation with genistein could attenuate these changes. These results implied that genistein could lower the elevated Hcy levels, and prevent the development of endothelial impairment in ovariectomized HHcy rats. This finding may shed a novel light on the anti-atherogenic activities of genistein in HHcy patients.
authors.affiliation: Department of Pathology, The Luhe Teaching Hospital of the Capital Medical University, 82 Xinhuanan Road, Tongzhou District, Beijing 101149, China.
authors.forename: Panpan
authors.initials: P
authors.lastname: Zhen
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhao
authors.forename: Dandan
authors.initials: D
authors.lastname: Hou
authors.forename: Teng
authors.initials: T
authors.lastname: Liu
authors.forename: Dongqiao
authors.initials: D
authors.lastname: Jiang
authors.forename: Jinhong
authors.initials: J
authors.lastname: Duan
authors.forename: Lingqiao
authors.initials: L
authors.lastname: Lu
authors.forename: Wen
authors.initials: W
authors.lastname: Wang
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D019332:Endothelin-1 / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology* / Q000648:ultrastructure; D004958:Estradiol / Q000097:blood; D005260:Female; D019833:Genistein / Q000494:pharmacology*; D006710:Homocysteine / Q000097:blood; D020138:Hyperhomocysteinemia / Q000097:blood / Q000473:pathology* / Q000503:physiopathology*; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects; D009599:Nitroprusside / Q000494:pharmacology; D010052:Ovariectomy; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D019332:Endothelin-1; D006710:Homocysteine; D009599:Nitroprusside; D010656:Phenylephrine; D004958:Estradiol; D008315:Malondialdehyde; D019833:Genistein; D000109:Acetylcholine