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Biochem Biophys Res Commun. 2017 Aug 12;490(1):36-43. doi: 10.1016/j.bbrc.2017.06.002. Epub 2017 Jun 2.

Taxifolin enhances osteogenic differentiation of human bone marrow mesenchymal stem cells partially via NF-κB pathway.

Author information

1
Department of Spine Surgery, Xiangya Hospital, Central South University, China.
2
Department of Spine Surgery, Xiangya Hospital, Central South University, China. Electronic address: zhq9996@163.com.
3
The State Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, China.

Abstract

Taxifolin, a flavonoid compound, has been reported to stimulate osteogenic differentiation in osteoblasts. The present study investigated whether taxifolin affects the osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) and the molecular mechanisms involved. The proliferation and osteogenic differentiation of hBMSCs in the presence of taxifolin were examined by CCK-8 assay, alkaline phosphatase (ALP) activity, ALP staining and Alizarin red staining. The expression of osteogenic differentiation markers were detected by real-time quantitative PCR (RT-PCR) analysis and western blot assay. The activation of potential related pathways was examined by luciferase reporter assay, immunofluorescence and western blot analysis. Taxifolin treatment increased osteogenic differentiation of hBMSCs without cytotoxicity. Luciferase reporter assay showed that taxifolin could not activate estrogen receptor pathway, but inhibit TNF-α-induced NF-κB signaling pathway activation in osteogenic induction condition. Moreover, the nucleus translocation of NF-κB under TNF-α treatment was inhibited by taxifolin treatment. The taxifolin-induced osteogenic differentiation effects of hBMSCs were abolished by TNF-α treatment. In conclusion, our results suggested that taxifolin could promote osteogenesis of hBMSCs, partially through antagonism of NF-κB signaling pathway.

KEYWORDS:

Flavonoid; MSC; NF-κB; Osteogenesis; Taxifolin

PMID:
28579433
DOI:
10.1016/j.bbrc.2017.06.002
[Indexed for MEDLINE]

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