Effect of GSK-137647A, the first non-carboxylic FFA4 agonist, on the osteogenic and adipogenic differentiation of bone mesenchymal stem cells in db/db mice.
Wang C., Liu Y., Pan Y., Jin H.
Animal Study, published in J Pharm Pharmacol (2019) — 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
- Animal Study
- Journal
- J Pharm Pharmacol (2019)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31858612
- DOI
- 10.1111/jphp.13217
Abstract (original English)
To investigate the effect of GSK-137647A, the first non-carboxylic FFA4 agonist, on osteogenic and adipogenic differentiation of bone mesenchymal stem cells (BMSCs) of db/db mice. Bone mesenchymal stem cells were extracted from 8-week-old db/db mice. Cell Counting Kit-8 was used to evaluate the toxicity of GSK-137647A on BMSCs, and the optimal concentration of GSK-137647A was selected to investigate the osteogenic and adipogenic differentiation of BMSCs, and relevant indicators of osteoblasts and adipocytes were detected. GSK-137647A had no significant toxicity on cell growth and proliferation. Moreover, GSK-137647A showed a significant increase in mineralization of BMSCs differentiated osteoblasts compared to the control group and elevated the alkaline phosphatase (ALP) activity in a time-dependent manner. Meanwhile, the treatment of GSK-137647A decreased the adipogenic differentiation of BMSCs. The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced. All of these results demonstrated that GSK-137647A suppressed the adipogenic differentiation and promoted osteogenic differentiation of BMSCs, which is partly attrib
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.
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