1. Ginsenoside-Rb2 Inhibits Dexamethasone-Induced Apoptosis Through Promotion of GPR120 Induction in Bone Marrow-Derived Mesenchymal Stem Cells.
- Author
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Gao, Bo, Huang, Qiang, Jie, Qiang, Zhang, Hong-Yang, Wang, Long, Guo, Yun-Shan, Sun, Zhen, Wei, Bo-Yuan, Han, Yue-Hu, Liu, Jian, Yang, Liu, and Luo, Zhuo-Jing
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MESENCHYMAL stem cells , *APOPTOSIS , *OSTEOPOROSIS , *G protein coupled receptors , *GINSENOSIDES , *DEXAMETHASONE , *EXTRACELLULAR signal-regulated kinases , *CELL survival - Abstract
Apoptosis of bone marrow-derived mesenchymal stem cells (BMMSCs) is an essential pathogenic factor of osteoporosis. Ginsenoside-Rb2 (Rb2), a 20(S)-protopanaxadiol glycoside extracted from ginseng, is a potent treatment for bone loss, which raises interest regarding the bone metabolism area. In the present study, we found that dose-response Rb2 inhibited high dosage of dexamethasone (Dex)-induced apoptosis in primary murine BMMSCs. Interestingly, Rb2 promoted GPR120 induction, which is the unsaturated long-chain fatty acid receptor. We further confirmed that GPR120-specific ShRNA reversed the inhibition of Rb2 on Dex-induced apoptosis by activating caspase-3 and reducing cell viability. In addition, Rb2 notably increased phosphorylated ERK1/2 levels and Ras kinase activity dependently through the GPR120. The ERK1/2 activity-specific inhibitor U0126 remarkably blocked the Rb2-induced antiapoptotic effect in response to Dex-induced apoptosis. Together, dose-response Rb2 protected BMMSCs against Dex-induced apoptosis dependently by inducing GPR120 promoted Ras-ERK1/2 signaling pathway. Therefore, in the prevalence of the abuse of Dex in the clinic, our findings suggest for the first time that Rb2 is not only a key to understand the link between Chinese medicine and the pathology of osteoporosis but also an underlying target for the treatment of bone complications in the foreseeable future. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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