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Ginsenoside-Rb2 inhibits dexamethasone-induced apoptosis through promotion of GPR120 induction in bone marrow-derived
Bo Gao1, Qiang Huang, Qiang Jie
1Institute of Orthopedic Surgery, Xijing Hospital, Fourth Military Medical University , Xi'an, People's Republic of China .
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.
Insights
Ginsenoside-Rb2 (Rb2) protects bone marrow stem cells from dexamethasone-induced apoptosis, a key factor in osteoporosis. This effect is mediated by the GPR120 receptor and the Ras-ERK1/2 pathway, offering potential therapeutic targets for bone loss.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Osteoporosis pathogenesis involves bone marrow-derived mesenchymal stem cell (BMMSC) apoptosis.
- Ginsenoside-Rb2 (Rb2), a ginseng extract, shows promise for treating bone loss.
- Dexamethasone (Dex) is frequently used clinically and can induce apoptosis in BMMSCs.
Purpose of the Study:
- To investigate the protective effects of Rb2 on Dex-induced BMMSC apoptosis.
- To elucidate the molecular mechanisms underlying Rb2's anti-apoptotic action.
Main Methods:
- Primary murine BMMSCs were treated with Rb2 and Dex.
- GPR120 expression was modulated using ShRNA.
- Caspase-3 activity, cell viability, and ERK1/2 phosphorylation were assessed.
- Ras kinase activity and ERK1/2 signaling pathway were analyzed.
Main Results:
- Rb2 inhibited Dex-induced apoptosis in BMMSCs in a dose-dependent manner.
- Rb2 upregulated GPR120 expression, which was crucial for its anti-apoptotic effect.
- Rb2 activated the Ras-ERK1/2 signaling pathway via GPR120 induction.
- Inhibition of GPR120 or ERK1/2 reversed the protective effects of Rb2.
Conclusions:
- Rb2 protects BMMSCs against Dex-induced apoptosis through the GPR120-mediated Ras-ERK1/2 signaling pathway.
- Rb2 represents a potential therapeutic agent for osteoporosis and related bone complications.
- This study highlights the link between traditional Chinese medicine and osteoporosis treatment.
