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

Wang, Yunjia; Zhang, Hongqi; Han, Hailong; Zou, Ying; Gao, Qi-Le; Yang, Guanteng

doi:10.1016/j.bbrc.2017.06.002

Cited by 40 publications

(47 citation statements)

References 28 publications

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“…The induction of NFATc1 upregulates the osteoclast-specific genes expression, such as TRAP, MMP-9, and CTK. Previous studies have shown, taxifolin exerted its biological effect via modulating NF-κB signaling [22,31]. In the present research, we observed that the taxifolin treatment inhibits the RANKL-induced NF-κB pathway activation, which was accomplished by the suppression of IκBα and NF-κB p65 phosphorylation.…”

Section: Discussionsupporting

confidence: 58%

“…Flavonoids may prevent bone loss by stimulate bone formation and inhibit bone resorption. Taxifolin, a flavonol with strong anti-oxidative effect, has been proven to promote osteogenic differentiation of human BMSCs in our previous research [22]. It has been proved that several other flavonoids and active components isolated from Chinese herb, such as scutellarin [23], schisantherin [24], tenuigenin [25], and gastrodin [26], inhibit osteoclast formation via RANKL or NFATc1 signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…As described in our previous research [22], BMCs collected by density gradient centrifugation from BM were cultured in α-MEM supplemented with 10% FBS. Floating cells were collected and further incubated with M-CSF (30 ng/mL) for 3 days.…”

Section: Bm Derived Macrophage Preparation and Osteoclastmentioning

confidence: 99%

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Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

et al. 2018

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It has been reported that taxifolin inhibit osteoclastogenesis in RAW264.7 cells. In our research, the inhibition effects of taxifolin on the osteoclastogenesis of human bone marrow-derived macrophages (BMMs) induced by receptor activator of NF-κB ligand (RANKL) as well as the protection effects in lipopolysaccharide-induced bone lysis mouse model have been demonstrated. In vitro, taxifolin inhibited RANKL-induced osteoclast differentiation of human BMMs without cytotoxicity. Moreover, taxifolin significantly suppressed RANKL-induced gene expression, including tartrate-resistant acid phosphatase, matrix metalloproteinase-9 nuclear factor of activated T cells 1 and cathepsin K, and F-actin ring formation. Further studies showed that taxifolin inhibit osteoclastogenesis via the suppression of the NF-κB signaling pathway. In vivo, taxifolin prevented bone loss in mouse calvarial osteolysis model. In conclusion, the results suggested that taxifolin has a therapeutic potential for osteoclastogenesis-related diseases such as osteoporosis, osteolysis, and rheumatoid arthritis.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

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Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

et al. 2018

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“…Recent studies have suggested that the inactivation of TLR-4 and NF-jB was involved in ECM synthesis and osteogenic differentiation (Wang et al 2017;Zhang, Hu, et al 2018). The results from the Western blot assay demonstrated that the expression of TLR-4 and P-65 phosphorylation was dramatically decreased in ACL fibroblasts by exposure to either PRP or SOWPa (100 mg/kg).…”

Section: Discussionmentioning

confidence: 98%

Positive effects of platelet-rich plasma (PRP) and a Sanguisorba officinalis polysaccharide on the proliferation and differentiation of anterior cruciate ligament (ACL) fibroblasts in vitro

Zheng

Huang²,

et al. 2020

Pharmaceutical Biology

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Context: Sanguisorba officinalis L. (Rosaceae), a famous traditional Chinese medicine. It was recently reported that its polysaccharide could facilitate collagen production. Objectives: We investigated the mechanism by which S. officinalis polysaccharide (SOWPa) and/or platelet-rich plasma (PRP) promote regenerative potential of anterior cruciate ligament (ACL) in vitro. Materials and methods: ACL fibroblasts were treated with SOWPa (25 and 100 mg/kg), PRP, PRP þ SOWPa (25 and 100 mg/kg) or vehicle alone for 24, 48, or 72 h. Cell viability, migration ability and apoptosis were evaluated by MTT, transwell and flow cytometry, respectively. Western blot analysis was performed to assess associated protein expression. Results: PRP, SOWPa (100 mg/kg) or PRP þ SOWPa (100 mg/kg) treatment for 72 h significantly improved the cell viability of ACL fibroblasts from 100 ± 7.5% (control) to 156.85 ± 12.82%, 188.08 ± 15.92%, and 223.67 ± 18.82%, respectively, which was evidenced by individual decreased apoptosis rate from 31.26 ± 2.35% (control) to 20.80 ± 1.89%, 18.01 ± 1.55% and 9.33 ± 0.78%. Furthermore, the motility of ACL fibroblasts was significantly improved with increased migrated cell number per field from 5 for control to 26 for PRP, 36 for SOWPa and 44 for PRP þ SOWPa, respectively. Moreover, the protein expression of differentiation markers (RUNX2, ALP, BMP2 and Col I) and TLR-4 and phosphorylated p65 (p-p65) was inhibited by the above treatment. Discussion and conclusions: Data suggested that the addition of SOWPa to PRP increased the regenerative ability of ACL fibroblasts by blocking the TLR-4/NF-jB pathway.

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“…However, whether this signaling pathway is activated or inhibited requires experimental confirmation. The nuclear factor-κB signaling pathway serves an important role in MSC differentiation into mature bone ( 42 ) and, therefore, its activity under the effects of naringin should be further investigated to advance the understanding of the molecular mechanism by which naringin affects MSCs.…”

Section: Discussionmentioning

confidence: 99%

Naringin promotes cellular chemokine synthesis and potentiates mesenchymal stromal cell migration via the Ras signaling pathway

Lin

Zhu

2018

Exp Ther Med

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Directional migration of mesenchymal stem cells (MSCs) is known to serve roles in bone fracture healing. Naringin is a traditional medicine used in China to treat bone injury and has been confirmed to act as a chemoattractant to MSCs. In the present study, the secretion of chemokines and stimulation of relevant signaling pathways by naringin were detected to determine the molecular mechanism of naringin-induced MSC migration. In these experiments, Quantibody® arrays were used to detect chemokines secreted by MSCs with or without the addition of naringin. The results revealed differential naringin-induced chemokine secretion of C-X-C motif chemokine (CXCL)5, CXCL6 and C-C motif chemokine 20. Furthermore, the Ras signaling pathway was markedly activated in the naringin-treated groups, suggesting that naringin may enhance the migrational ability of MSCs via Ras activation. Furthermore, naringin was able to promote the secretion of various chemokines derived from MSCs, which would, in turn, increase the mobility of MSCs. The aim of the present study was to provide novel candidate agents for clinical orthopedics and theoretical basis for the future improvement of adjunctive medication for bone fracture healing.

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

Cited by 40 publications

References 28 publications

Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

Positive effects of platelet-rich plasma (PRP) and a Sanguisorba officinalis polysaccharide on the proliferation and differentiation of anterior cruciate ligament (ACL) fibroblasts in vitro

Naringin promotes cellular chemokine synthesis and potentiates mesenchymal stromal cell migration via the Ras signaling pathway

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