Puerarin promotes the proliferation and differentiation of MC3T3-E1 cells via microRNA-106b by targeting receptor activator of nuclear factor-κB ligand
Shan Z., Cheng N., Huang R., Zhao B., Zhou Y.
Laboratory Study, published in Exp Ther Med (2018) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Exp Ther Med (2018)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 29375675
- PMCID
- PMC5766078
- DOI
- 10.3892/etm.2017.5405
- Citations
- 13
Abstract (original English)
Puerarin, an isoflavone-C-glucoside extracted from the root of Pueraria Labata (Willd.) Ohwi, is one of the most important crude herbs used in Chinese medicine for various medicinal purposes. Accumulating evidence has indicated that puerarin suppresses bone resorption and promotes bone formation. However, the molecular mechanism involved in puerarin-associated bone formation is unclear. The present study aimed to investigate the molecular mechanism of puerarin-induced osteoblast proliferation and differentiation. The study showed that puerarin treatment differentially affected cell proliferation in a time-dependent manner. Notably, at a concentration of 20 µM, puerarin significantly promoted cell proliferation in comparison with the control (P<0.01). Furthermore, puerarin promoted MC3T3-E1 cell differentiation at an appropriate concentration. In addition, miR-106b was significantly upregulated in MC3T3-E1 cells following treatment with 20 µM puerarin (P<0.01), and a known target for miR-106b, receptor activator of nuclear factor-κB ligand (RANKL) was demonstrated using the luciferase reporter assay. Furthermore, inhibition of miR-106b significantly reversed the promotion of cell differentiation induced by puerarin in MC3T3-E1 cells (P<0.01). In conclusion, the present study demonstrated that puerarin exerts its role in MC3T3-E1 osteogenesis through miR-106b by targeting RANKL.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.