Chrysin promotes osteogenic differentiation via ERK/MAPK activation.
10.1007/s13238-013-3003-3
- Author:
Wenfeng ZENG
1
;
Yan YAN
;
Fayun ZHANG
;
Chunling ZHANG
;
Wei LIANG
Author Information
1. Protein & Peptide Pharmaceutical Laboratory, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Cell Differentiation;
drug effects;
Cell Line;
Enzyme Activation;
drug effects;
Flavonoids;
pharmacology;
therapeutic use;
Mice;
Mitogen-Activated Protein Kinase 1;
metabolism;
Mitogen-Activated Protein Kinase 3;
metabolism;
Mitogen-Activated Protein Kinases;
metabolism;
Osteoblasts;
drug effects;
pathology;
Osteogenesis;
drug effects;
Osteoporosis;
drug therapy;
pathology;
Phosphorylation;
drug effects;
Receptors, Estrogen;
metabolism
- From:
Protein & Cell
2013;4(7):539-547
- CountryChina
- Language:English
-
Abstract:
The effect of the anti-inflammatory flavonoid chrysin on osteogenesis was determined in preosteoblast MC3T3-E1 cells. Results demonstrated that chrysin could induce osteogenic differentiation in the absence of other osteogenic agents. Chrysin treatment promoted the expression of transcription factors (Runx2 and Osx) and bone formation marker genes (Col1A1, OCN, and OPN) as well as enhanced the formation of mineralized nodules. During osteogenic differentiation, chrysin preferentially activated ERK1/2, but not JNK nor the p38 MAPKs. Further experiments with inhibitors revealed the co-treatment of U0126, PD98059, or ICI182780 (a general ER antagonist) with chrysin effectively abrogated the chrysin-induced osteogenesis and ERK1/2 activation. Thus, the effect of chrysin on osteogenesis is ERK1/2-dependent and involves ER. Therefore, chrysin has the significant potential to enhance osteogenesis for osteoporosis prevention and treatment.
