Puerarin enhances proliferation and osteoblastic differentiation of human bone marrow stromal cells via a nitric oxide/cyclic guanosine monophosphate signaling pathway

Lv, Haihong; Che, Tuanjie; Tang, Xulei; Liu, Lijuan; Cheng, Jianguo

doi:10.3892/mmr.2015.3647

Cited by 16 publications

(12 citation statements)

References 38 publications

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“…Through functional enrichment, we identified that NO can induce multiple molecular pathways such as protein kinase activity, estrogen receptor activity, BMP receptor binding, ligand-gated ion channel activity, or phosphatidylinositol 3-phosphate binding. Consistent with our results, many studies have demonstrated the relationship between NO and estrogen receptor signaling in several biological processes including osteogenic development [44][45][46]. Moreover, BMP signaling-induced NO production stimulated bone calcification in zebrafish [47].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andsupporting

confidence: 80%

Osteogenic Effect of Inducible Nitric Oxide Synthase (iNOS)-Loaded Mineralized Nanoparticles on Embryonic Stem Cells

Lee¹,

Lee²,

Lee³

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study investigated the effect of inducible nitric oxide synthase-loaded mineralized nanoparticles (iNOS-MNPs) on the osteogenic differentiation of mouse embryonic stem cells (ESCs). Methods: We prepared iNOS-MNPs using an anionic block copolymer template-mediated calcium carbonate (CaCO₃) mineralization process in the presence of iNOS. iNOS-MNPs were spherical and had a narrow size distribution. iNOS was stably loaded within MNPs without denaturation. In order to confirm the successful introduction of iNOS-MNPs into the cytosol of ESCs, intracellular levels of nitric oxide (NO) was determined with a fluorometric analysis. A NO effector molecule, cyclic guanosine 3’,5’ monophosphate (cGMP) was also quantified with a competitive enzyme immunoassay. Cell viability in response to iNOS-MNP treatment was determined using the cell counting kit-8 (CCK-8) assay. Alkaline phosphatase (ALP) activity assay, intracellular calcium quantification assay, and Alizarin red S staining for matrix mineralization were performed to investigate osteogenic differentiation of ESCs. The protein levels of Runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), and osterix (OSX) as osteogenic-related factors were also assessed by immunofluorescence staining and Western blot analysis. The complex pathways associated with iNOS-MNP-derived osteogenic differentiation of ESCs were evaluated by network-based analysis. Results: Cells with iNOS-MNPs displayed a significant increase in NO and cGMP concentration compared with the control group. When cells were exposed to iNOS-MNPs, there were no adverse effects on cell viability. Importantly, iNOS-MNP uptake promoted the osteogenic differentiation of ESCs. Using transcriptome profiling, we obtained 1,836 differentially-induced genes and performed functional enrichment analysis with ClueGO and KEGG. These analyses identified significantly enriched and interconnected molecular pathways such as protein kinase activity, estrogen receptor activity, bone morphogenetic protein (BMP) receptor binding, ligand-gated ion channel activity, and phosphatidylinositol 3-phosphate binding. Conclusion: These findings suggest that iNOS-MNPs can induce osteogenic differentiation in ESCs by integrating complex signaling pathways.

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Section: Cellular Physiology and Biochemistry Cellular Physiology Andsupporting

confidence: 80%

Osteogenic Effect of Inducible Nitric Oxide Synthase (iNOS)-Loaded Mineralized Nanoparticles on Embryonic Stem Cells

Lee¹,

Lee²,

Lee³

et al. 2018

Cell Physiol Biochem

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“…The increased synthesis of DNA may reflect more activities of cell proliferation. Previous studies have reported that puerarin enhanced the proliferation of human bone marrow stromal cells, and attenuated the proliferation of diabetes-induced vascular smooth muscle cells and bladder cancer cells [43][44][45], all of which is also beneficial to animals.…”

Section: Discussionmentioning

confidence: 96%

Dietary Puerarin Supplementation Alleviates Oxidative Stress in the Small Intestines of Diquat-Challenged Piglets

Yuan

Liu

et al. 2020

Animals

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This study was conducted to demonstrate that dietary puerarin supplementation alleviates oxidative stress in the small intestine of diquat-challenged piglets. The results showed that puerarin administration markedly alleviated diquat-induced intestinal injury, which was indicated by the improvement of intestinal morphology, cell proliferation and barrier function. One of the potential mechanisms responsible for this was the decrease in oxidative stress, as evidenced by the increase in activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) in the small intestine. Puerarin increased the protein expression levels of NF-E2-related factor 2 (Nrf2) and its downstream enzymes, including heme oxygenase 1 (HO-1), glutamate–cysteine ligase catalytic and its modifier subunit (GCLc and GCLm) in the jejunal mucosa of diquat-induced piglets. Puerarin administration improved intestinal morphology, cell proliferation, and barrier function, and increased Nrf2 and its downstream enzymes. These findings indicate that the dietary supplementation of puerarin attenuates the oxidative stress involving Nrf2 signaling pathways in diquat-challenged piglets.

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“…Several reports have demonstrated that puerarin is able to promote osteoblast proliferation and differentiation ( 29 , 30 ). A study from Wong and Rabie ( 31 ) showed that puerarin treatment may prevent bone loss in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Puerarin promotes the proliferation and differentiation of MC3T3-E1 cells via microRNA‑106b by targeting receptor activator of nuclear factor‑κB ligand

et al. 2017

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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. The findings suggest that puerarin may be considered a promising anti-osteoporotic agent for the treatment of osteoporosis.

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Puerarin enhances proliferation and osteoblastic differentiation of human bone marrow stromal cells via a nitric oxide/cyclic guanosine monophosphate signaling pathway

Cited by 16 publications

References 38 publications

Osteogenic Effect of Inducible Nitric Oxide Synthase (iNOS)-Loaded Mineralized Nanoparticles on Embryonic Stem Cells

Osteogenic Effect of Inducible Nitric Oxide Synthase (iNOS)-Loaded Mineralized Nanoparticles on Embryonic Stem Cells

Dietary Puerarin Supplementation Alleviates Oxidative Stress in the Small Intestines of Diquat-Challenged Piglets

Puerarin promotes the proliferation and differentiation of MC3T3-E1 cells via microRNA‑106b by targeting receptor activator of nuclear factor‑κB ligand

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