4.7 Article

Bu-Gu-Sheng-Sui decoction promotes osteogenesis via activating the ERK/Smad signaling pathways

期刊

FRONTIERS IN PHARMACOLOGY
卷 13, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2022.976121

关键词

Bu-Gu-Sheng-Sui decoction; osteogenesis; mechanism; ERK; Smad; osteoporosis

资金

  1. General Project of the National Natural Science Foundation of China
  2. Fundamental Research Funds for the Central Public Welfare Research Institutes
  3. [81704102]

向作者/读者索取更多资源

This study investigated the effects of Bu-Gu-Sheng-Sui decoction (BGSSD) on osteogenesis and its potential mechanism. The results showed that BGSSD protected bone mass, increased the expression of osteogenic specific factor Runx2, and improved bone trabecular structure. In vitro, BGSSD accelerated the proliferation and differentiation of MC3T3-E1 cells and increased the expression of Runx2. Moreover, BGSSD effectively boosted the expression levels of ERK and Smad. These findings suggest that BGSSD may promote bone formation through the ERK/Smad pathways.
Osteoporosis is a systemic metabolic skeletal disease, which becomes a common public health problem that seriously endangers people's health. Bu-Gu-Sheng-Sui decoction (BGSSD) is a safe and effective Chinese medicine formulation for the treatment of osteoporosis. Numerous studies have indicated that it played a significant role in bone anabolism. However, the underlying mechanism remains unclear. Herein, we selected senescence-accelerated mice prone 6 (SAMP6) and MC3T3-E1 cells to study the effects of BGSSD on osteogenesis and then investigated the potential mechanism of BGSSD. Our research found that BGSSD protected the bone mass in SAMP6, increased the expression of osteogenic specific factor Runx2, and improved bone trabecular structure. In vitro, BGSSD accelerated the proliferation and differentiation of MC3T3-E1 cells, which was characterized by stimulating the activity of Alkaline phosphatase (ALP) and raising the expression of Runx2. Moreover, BGSSD could effectively boost the expression levels of ERK and Smad in SAMP6 and MC3T3-E1. Therefore, we speculate that BGSSD may promote bone formation through ERK/Smad pathways. Collectively, our results highlight the importance of BGSSD as a compound in promoting osteogenic differentiation and osteogenesis, demonstrating that BGSSD may become a latent drug to prevent and treat osteoporosis.

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