Curcumin represses adipogenic differentiation of human bone marrow mesenchymal stem cells via inhibiting kruppel-like factor 15 expression.
Wang T., Yan R., Xu X., Li X., Cao L., Gao L.
Laboratory Study on Systemic / IV, published in Acta Histochem (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
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- Study type
- Laboratory Study
- Journal
- Acta Histochem (2019)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 30611528
- DOI
- 10.1016/j.acthis.2018.12.007
Abstract (original English)
Understanding the mechanisms of adipogenic differentiation may lead to the discovery of novel therapeutic targets for obesity. The natural plant polyphenol compound curcumin can improve obesity-associated inflammation and diabetes in obese mice. The role of curcumin in adipogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs) is still unclear. We used hMSCs to investigate the details of the mechanism underlying the adipogenic effects of curcumin. At different time points (i.e., 5 days and 10 days) of hMSC adipocyte differentiation, an accumulation of large lipid droplets was analyzed in Oil Red O-stained cultured cells in two curcumin (5 μM and 10 μM) groups and the control group. The cells were also harvested for the detection of mRNA and protein expressions by quantitative real-time polymerase chain reaction and Western blot analysis. The results showed that curcumin can suppresses adipocyte differentiation in a dose-dependent manner and inhibited the expression of PPARγ, C/EBPα, and FABP4. Importantly, curcumin can also suppress the expression of Kruppel-like factor 15, which may bind to the PPARγ promoter, resulting in downregulation of PPARγ expression to inhibit the adipogenic differentiation of hMSCs.
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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