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Nutr Res. 2017 Jun;42:20-30. doi: 10.1016/j.nutres.2017.04.009. Epub 2017 May 6.

Daidzein stimulates osteogenesis facilitating proliferation, differentiation, and antiapoptosis in human osteoblast-like MG-63 cells via estrogen receptor-dependent MEK/ERK and PI3K/Akt activation.

Author information

1
Tianjin Key Laboratory for Prevention and Control of Occupational and Environmental Hazard, Tianjin 300309, China; Department of Pharmacology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: jinxin1227@126.com.
2
Department of Pharmacology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: sunjingsj2001@sina.com.
3
Department of Pathogenic Biology and Immunology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: 2457274460@qq.com.
4
Tianjin Key Laboratory for Prevention and Control of Occupational and Environmental Hazard, Tianjin 300309, China; Department of Pathogenic Biology and Immunology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: wangyue6808@126.com.
5
Department of Medical Administration, The General Hospital of Chinese People's Armed Police Force, Beijing 100039, China. Electronic address: niuniu19842006@163.com.
6
Department of Pathogenic Biology and Immunology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: yangjingdj@hotmail.com.
7
Department of Pathogenic Biology and Immunology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: sufi1209@126.com.
8
Department of Pharmacology, Logistics University of Chinese People's Armed Police Force, Tianjin 300309, China. Electronic address: 2236021259@qq.com.

Abstract

Daidzein, a natural soy isoflavone, has a structure similar to estradiol and exhibiting bone-sparing effects against osteoporosis. However, the molecular mechanisms of osteogenesis remain unclear. We hypothesized that daidzein stimulates osteogenesis through estrogen receptor (ER)-dependent signal pathways. To test this hypothesis, we investigated the effects of daidzein compared with 17β-estradiol on proliferation, differentiation, and cisplatin-induced apoptosis in human osteoblast-like MG-63 cells containing 2 ER isoforms. The results showed that daidzein stimulated cell proliferation by altering cell cycle distribution, promoted cell differentiation by increasing the alkaline phosphatase activity and collagen content, and reduced cell apoptosis associated by up-regulating the expression of Bcl-xL. The above actions of daidzein were prevented by cotreatment with the ER antagonist ICI 182780. Using small interfering RNA technology, we further demonstrated that the effects of daidzein on alkaline phosphatase activity, collagen content, and cell apoptosis are mediated by both ERα and ERβ, whereas the effects on cell proliferation are primarily mediated by ERα. However, the effects of 17β-estradiol on osteoblastic proliferation and survival are mediated by both ER isotypes, and the effects on osteoblastic differentiation are primarily mediated by ERα. The use of specific inhibitors indicated that activation of the mitogen-activated protein kinase kinase/extracellular regulated kinase (MEK/ERK) and phosphoinositide 3-kinase/protein kinase B or PKB (PI3K/Akt) signaling pathway at least partially accounts for these effects of daidzein. Taken together, the results indicate that daidzein stimulates osteogenesis through facilitating proliferation, differentiation, and antiapoptosis in human osteoblast-like MG-63 cells via activation of MEK/ERK and PI3K/Akt in an ER-dependent manner.

KEYWORDS:

Apoptosis; Daidzein; Differentiation; Estrogen receptor; Osteoblast; Proliferation

PMID:
28633868
DOI:
10.1016/j.nutres.2017.04.009
[Indexed for MEDLINE]

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