Coumarins from <i>Cnidium monnieri</i> and their Antiosteoporotic Activity

Zhang, Qiaoyan; Qin, Lu‐Ping; Wang, He; Puyvelde, Luc Van; Maes, Dominick; Adams, An; Zheng, Huabin; Kimpe, Norbert De

doi:10.1055/s-2006-951724

Cited by 100 publications

(51 citation statements)

References 16 publications

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“…It has been reported that Osthole promoted the differentiation and maturation of osteoblasts [11][12][13][14]. However, our observations in this study seem controdictory to other reported findings, which are as follows: Firstly, the MSC proliferation was inhibited by Osthole.…”

Section: Cell Physiolcontrasting

confidence: 85%

“…It had been widely reported that Osthole exerts a significant positive effect on osteoporosis treatment by promoting osteoblast differentiation and inhibiting bone resorption [10][11][12][13][14]. Interestingly, a recent study on biomaterial suggested that Osthole stimulation may enhance extracellular matrix (ECM) production and positively affect cell behavior in cell sheet engineering of jaw bone marrow mesenchymal stem cells [15].…”

Section: Introductionmentioning

confidence: 99%

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An Inhibitory Role of Osthole in Rat MSCs Osteogenic Differentiation and Proliferation via Wnt/β-Catenin and Erk1/2-MAPK Pathways

Chen

Dai

et al. 2016

Cell Physiol Biochem

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Background/Aims: Bone marrow-derived mesenchymal stem cells (MSCs) are responsible for new bone formation during adulthood. Accumulating evidences showed that Osthole promotes the osteogenic differentiation in primary osteoblasts. The aim of this study was to investigate whether Osthole exhibits a potential to stimulate the osteogenic differentiation of MSCs and the underlying mechanism. Methods: MSCs were treated with a gradient concentration of Osthole (6.25 µM, 12.5 µM, and 25 µM). Cell proliferation was assessed by western blotting with the proliferating cell nuclear antigen (PCNA) and Cyclin D1 antibodies, fluorescence activated cell sorting (FACS), and cell counting kit 8 (CCK8). MSCs were cultured in osteogenesis-induced medium for one or two weeks. The osteogenic differentiation of MSCs was estimated by Alkaline Phosphatase (ALP) staining, Alizarin red staining, Calcium influx, and quantitative PCR (qPCR). The underlying mechanism of Osthole-induced osteogenesis was further evaluated by western blotting with antibodies in Wnt/β-catenin, PI3K/Akt, BMPs/smad1/5/8, and MAPK signaling pathways. Results: Osthole inhibited proliferation of rat MSCs in a dose-dependent manner. Osthole suppressed osteogenic differentiation of rat MSCs by down-regulating the activities of Wnt/β-catenin and Erk1/2-MAPK signaling. Conclusions: Osthole inhibits the proliferation and osteogenic differentiation of rat MSCs, which might be mediated through blocking the Wnt/β-catenin and Erk1/2-MAPK signaling pathways.

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Section: Cell Physiolcontrasting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

An Inhibitory Role of Osthole in Rat MSCs Osteogenic Differentiation and Proliferation via Wnt/β-Catenin and Erk1/2-MAPK Pathways

Chen

Dai

et al. 2016

Cell Physiol Biochem

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“…Its chemical formula is C 15 H 16 O 3 . Osthole has been shown to exert a wide variety of biological effects, such as anti-seizure, anti-osteoporosis and anti-inflammation [10,11,12,13]. It has been well documented that osthole inhibits the growth and proliferation of various cancer cells through inducing apoptosis or cell cycle arrest [14,15].…”

Section: Introductionmentioning

confidence: 99%

Osthole Induces Cell Cycle Arrest and Inhibits Migration and Invasion via PTEN/Akt Pathways in Osteosarcoma

Wang

Lei

et al. 2016

Cell Physiol Biochem

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Background/Aims: Osteosarcoma is the second highest cause of cancer-related death in children and adolescents. Majority of osteosarcoma patients (90%) show metastasis. Previous reports revealed that osthole showed antitumor activities via induction of apoptosis and inhibition of proliferation. However, the potential effects and detailed molecular mechanisms involved remained unclear. Methods: Cell viability was analyzed by MTT assay in osteosarcoma cell lines MG-63 and SAOS-2. Cell cycle was detected by flow cytometry. The effects of migration and invasion were evaluated by wound healing assay and transwell assays. Moreover, the level of proteins expression was determined by Western blot. Results: The cell viability of MG63 and SAOS-2 were markedly inhibited by osthole in a dose- and time-dependent manner. Cell cycle was arrested and the ability of migration and invasion was obviously reduced when cells were exposed to osthole. Moreover, enzymes involved in PTEN/Akt pathway were regulated such as PTEN and p-Akt proteins. Furthermore, osthole inhibited the tumor growth in vivo. Conclusion: Our study unraveled, for the first time, the ability of osthole to suppress osteosarcoma and elucidated the regulation of PTEN/Akt pathway as a signaling mechanism for the anti-tumor action of osthole. These findings indicate that osthole may represent a novel therapeutic strategy in the treatment of osteosarcoma.

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“…Furthermore, the effective concentration of bergapten (20-40 μmol/L) on LPS-induced bone loss in vitro was higher than that of it on osteoblast-like cells (such as UMR106, MG 63 and hFOB) (0.3-10 μmol/L) [10,11], indicating that bergapten preventing LPS-induced bone loss requires stronger concentrations than that of its stimulation of bone formation required in vitro. However, Zhang et al reported that bergapten had no effect on separated mature osteoclast and osteoclast resorption [17]. These different experimental results require further study.…”

Section: Discussionmentioning

confidence: 95%

Bergapten prevents lipopolysaccharide mediated osteoclast formation, bone resorption and osteoclast survival

Zheng

et al. 2013

International Orthopaedics (SICOT)

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Purpose This study was designed to investigate the potential effect of bergapten on lipopolysaccharide (LPS)-mediated osteoclast formation, bone resorption and osteoclast survival in vitro. Methods After osteoclast precursor RAW264.7 cells were treated with bergapten (5, 20, 40 μmol/L) for 72 hours in the presence of LPS (100 ng/ml), osteoclastogenesis was identified by tartrate-resistant acid phosphatase (TRAP) staining, and the number of TRAP-positive multinucleated cells [TRAP(+ )MNCs] per well were counted. To investigate the effect of bergapten on osteoclastic bone resorption, RAW264.7 cells were treated with bergapten for six days in the presence of LPS, and the area of bone resorption was analyzed with Image Pro-Plus. Next, we examined apoptosis of RAW264.7 cells after bergapten incubation for 48 hours by flow cytometer using annexin V/propidium iodide (PI) double labeling. Finally, osteoclast survival was observed by Hoechst 33342 labeling and Western blotting after bergapten treatment for 24 hours. Results Data showed that bergapten (5-40 μmol/L) dosedependently inhibited LPS-induced osteoclast formation and bone resorption. Treatment with bergapten triggered apoptotic death of osteoclast precursor RAW264.7 cells in a dosedependent manner. Furthermore, bergapten significantly reduced the survival of mature osteoclast, as demonstrated by emergence of apoptotic nuclei and activation of apoptotic protein caspase 3/9.Conclusions These findings suggest that bergapten effectively prevents LPS-induced osteoclastogenesis, bone resorption and survival via apoptotic response of osteoclasts and their precursors. The study identifies bergapten as an inhibitor of osteoclast formation and bone resorption and provides evidence that bergapten might be beneficial as an alternative for prevention and treatment of inflammatory bone loss.

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Coumarins from Cnidium monnieri and their Antiosteoporotic Activity

Cited by 100 publications

References 16 publications

An Inhibitory Role of Osthole in Rat MSCs Osteogenic Differentiation and Proliferation via Wnt/β-Catenin and Erk1/2-MAPK Pathways

An Inhibitory Role of Osthole in Rat MSCs Osteogenic Differentiation and Proliferation via Wnt/β-Catenin and Erk1/2-MAPK Pathways

Osthole Induces Cell Cycle Arrest and Inhibits Migration and Invasion via PTEN/Akt Pathways in Osteosarcoma

Bergapten prevents lipopolysaccharide mediated osteoclast formation, bone resorption and osteoclast survival

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