淫羊藿苷
骨保护素
雌激素受体
化学
雌激素
兰克尔
内科学
内分泌学
雌激素受体α
激活剂(遗传学)
雌激素受体
受体
成骨细胞
药理学
细胞生物学
生物化学
生物
体外
医学
乳腺癌
替代医学
病理
癌症
作者
Hui Xi,Chung Yan Fung,Sao King Mok,Ka-Chun Wong,Ming Xian Ho,Xin Luan Wang,Xin Yao,Man Sau Wong
标识
DOI:10.1016/j.jsbmb.2014.02.019
摘要
Total flavonoids in Herba epimedii (HEP) have been demonstrated to protect against bone loss and bone deterioration associated with estrogen deficiency without exerting any uterotrophic effects. However, it is unclear how flavonoids in HEP exert their protective effects on bone and if different flavonoids exert estrogenic actions in bone cells via similar mechanism of actions. The present study aims to investigate the bone anabolic effects of four major flavonoids isolated from HEP, namely icariin, baohuoside-I, epimedin B and sagittatoside A as well as the mechanism involved in mediating their estrogenic actions in rat osteoblastic-like UMR-106 cells. All tested compounds significantly stimulated the cell proliferation rate, alkaline phosphate (ALP) activity and osteoprotegerin (OPG)/receptor activator of nuclear factor κ-B ligand (RANKL) mRNA expression in UMR-106 cells and their effects could be abolished by co-incubation with 10−6 M ICI 182,780. None of the flavonoids exhibited binding affinities toward ERα and ERβ. However, sagittatoside A selectively activated estrogen response element (ERE)-luciferase activity via ERα. In addition, icariin and sagittatoside A induced ERα phosphorylation at serine 118 residue. Taken together, our results indicated that all four flavonoids from HEP stimulated ER-dependent osteoblastic functions in UMR-106 cells, but only two of them appeared to exert their actions by ligand-independent activation of ERα. Our study provides evidence to support the hypothesis that the estrogen-like protective effects on bone by flavonoids are mediated via mechanisms that are distinct from the classical actions of estrogen.
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