ERα36 is involved in the proliferation promotion and anti-apoptosis effects of icaritin on MG63 cells.
- Author:
Wei LIU
1
;
Zi-Qiang LUO
2
;
Lu REN
1
;
Mei SUN
1
;
Ju-Qin YAO
1
;
Jing-Xia WANG
1
;
Zun WANG
1
;
Si-Yuan TANG
3
Author Information
1. Xiangya Nursing School, Central South University, Changsha 410000, China.
2. School of Basic Medical Science, Central South University, Changsha 410000, China.
3. Xiangya Nursing School, Central South University, Changsha 410000, China. sytang263@outlook.com.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2018;70(5):474-480
- CountryChina
- Language:Chinese
-
Abstract:
The mechanism for icaritin to improve postmenopausal osteoporosis (PMOP) has not been clarified. The aim of this study was to investigate the role of estrogen receptor α36 (ERα36) in the proliferation promotion and anti-apoptosis effects of icaritin on osteoblasts and the underlying mechanism of downstream signal transduction. The ERα36 knockdown human osteosarcoma MG63 cell model was constructed by transfection of shRNA vector. Cell proliferation was detected by CCK-8, the apoptosis was detected by flow cytometry, and the activation of ERK and AKT signaling pathways was detected by Western blot. The results showed that the effects of icaritin on the proliferation and apoptosis of MG63 cells were significantly decreased after ERα36 knockdown, and icaritin could up-regulate the levels of ERK and AKT phosphorylation in MG63 cells, which could be reduced by ERα36 knockdown. The effect of icaritin on the proliferation of MG63 cells was significantly decreased by pretreating the cells with U0126 (an ERK signaling pathway blocker) and LY294002 (an AKT signaling pathway blocker), respectively. Furthermore, anti-apoptotic effect of icaritin on MG63 cells was significantly decreased after the cells were pretreated with U0126, but not with LY294002. These results suggest that icaritin exerts proliferation promotion and anti-apoptosis effects on osteoblasts through ERα36 and its downstream ERK and AKT signaling pathways.
