scholarly journals Rosmarinic acid and arbutin suppress osteoclast differentiation by inhibiting superoxide and NFATc1 downregulation in RAW 264.7 cells

2015 ◽  
Vol 3 (4) ◽  
pp. 483-490 ◽  
Author(s):  
AKINA OMORI ◽  
YOSHITAKA YOSHIMURA ◽  
YOSHIAKI DEYAMA ◽  
KUNIAKI SUZUKI
Keyword(s):  
Rosmarinic Acid ◽  
Osteoclast Differentiation ◽  
Raw 264.7 Cells ◽  
Raw 264.7

scholarly journals Crataegus pinnatifida Bunge Inhibits RANKL-Induced Osteoclast Differentiation in RAW 264.7 Cells and Prevents Bone Loss in an Ovariectomized Rat Model

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Minsun Kim ◽  
MinBeom Kim ◽  
Jae-Hyun Kim ◽  
SooYeon Hong ◽  
Dong Hee Kim ◽  
...  
Keyword(s):  
Bone Loss ◽  
Rat Model ◽  
Osteoclast Differentiation ◽  
Ovariectomized Rat ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Mineral Density ◽  
Crataegus Pinnatifida

Osteoporosis is characterized by a decrease in bone microarchitecture with an increased risk of fracture. Long-term use of primary treatments, such as bisphosphonates and selective estrogen receptor modulators, results in various side effects. Therefore, it is necessary to develop alternative therapeutics derived from natural products. Crataegus pinnatifida Bunge (CPB) is a dried fruit used to treat diet-induced indigestion, loss of appetite, and diarrhea. However, research into the effects of CPB on osteoclast differentiation and osteoporosis is still limited. In vitro experiments were conducted to examine the effects of CPB on RANKL-induced osteoclast differentiation in RAW 264.7 cells. Moreover, we investigated the effects of CPB on bone loss in the femoral head in an ovariectomized rat model using microcomputed tomography. In vitro, tartrate-resistant acid phosphatase (TRAP) staining results showed the number of TRAP-positive cells, and TRAP activity significantly decreased following CPB treatment. CPB also significantly decreased pit formation. Furthermore, CPB inhibited osteoclast differentiation by suppressing NFATc1, and c-Fos expression. Moreover, CPB treatment inhibited osteoclast-related genes, such as Nfatc1, Ca2, Acp5, mmp9, CtsK, Oscar, and Atp6v0d2. In vivo, bone mineral density and structure model index were improved by administration of CPB. In conclusion, CPB prevented osteoclast differentiation in vitro and prevented bone loss in vivo. Therefore, CPB could be a potential alternative medicine for bone diseases, such as osteoporosis.

Edgeworthia papyrifera Regulates Osteoblast and Osteoclast Differentiation In Vitro and Exhibits Anti-osteoporosis Activity in Animal Models of Osteoporosis

Planta Medica ◽  
2019 ◽  
Vol 85 (09/10) ◽  
pp. 766-773 ◽  
Author(s):  
Pansoo Kim ◽  
Yeon-Ju Nam ◽  
Woo Jung Kim ◽  
Jin Kyu Kim ◽  
Gyeongbeen Lee ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Animal Models ◽  
Osteoclast Differentiation ◽  
Raw 264.7 Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Raw 264.7 ◽  
Treatment Of Osteoporosis ◽  
Increased Risk ◽  
Interesting Candidate

AbstractOsteoporosis is a clinical condition characterized by low bone strength that leads to an increased risk of fracture. Strategies for the treatment of osteoporosis involve inhibition of bone resorption by osteoclasts and an increase of bone formation by osteoblasts. Here, we identified the extract derived from the stem part of Edgeworthia papyrifera that enhanced differentiation of MC3T3-E1 cells to osteoblast-like cells and inhibited osteoclast differentiation of RAW 264.7 cells in vitro. In support of our observation, rutin and daphnoretin, which were previously reported to inhibit osteoclast differentiation, were identified in E. papyrifera extract. In an animal model of osteoporosis, the ovariectomy-induced increases in bone resorption biomarkers such as pyridinoline and tartrate-resistant acid phosphatase were significantly reduced by E. papyrifera extract administration at 25.6 and 48.1%, respectively. Furthermore, the ovariectomy-induced bone loss in animal models of osteoporosis was significantly prevented by the administration of E. papyrifera in our study. Taking these observations into account, we suggest that E. papyrifera is an interesting candidate for further exploration as an anti-osteoporotic agent.

scholarly journals The effects of Lycii Radicis Cortex on RANKL-induced osteoclast differentiation and activation in RAW 264.7 cells

2016 ◽  
Vol 37 (3) ◽  
pp. 649-658 ◽  
Author(s):  
JAE-HYUN KIM ◽  
EUN-YOUNG KIM ◽  
BINA LEE ◽  
JU-HEE MIN ◽  
DEA-UK SONG ◽  
...  
Keyword(s):  
Osteoclast Differentiation ◽  
Raw 264.7 Cells ◽  
Raw 264.7

scholarly journals Fermented Sea Tangle (Laminaria japonica Aresch) Suppresses RANKL-Induced Osteoclastogenesis by Scavenging ROS in RAW 264.7 Cells

Foods ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 290
Author(s):  
Jeong ◽  
Ji ◽  
Lee ◽  
Hong ◽  
Kim ◽  
...  
Keyword(s):  
Osteoclast Differentiation ◽  
Laminaria Japonica ◽  
Asia Pacific ◽  
Raw 264.7 Cells ◽  
Marker Genes ◽  
Raw 264.7 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Food Ingredient ◽  
Laminaria Japonica Aresch

Sea tangle (Laminaria japonica Aresch), a brown alga, has been used for many years as a functional food ingredient in the Asia-Pacific region. In the present study, we investigated the effects of fermented sea tangle extract (FST) on receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-stimulated osteoclast differentiation, using RAW 264.7 mouse macrophage cells. FST was found to inhibit the RANKL-stimulated activation of tartrate-resistance acid phosphatase (TRAP) and F-actin ring structure formation. FST also down-regulated the expression of osteoclast marker genes like TRAP, matrix metalloproteinase-9, cathepsin K and osteoclast-associated receptor by blocking RANKL-induced activation of NF-κB and expression of nuclear factor of activated T cells c1 (NFATc1), a master transcription factor. In addition, FST significantly abolished RANKL-induced generation of reactive oxygen species (ROS) by activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and its transcriptional targets. Hence, it seems likely that FST may have anti-osteoclastogenic potential as a result of its ability to inactivate the NF-κB-mediated NFATc1 signaling pathway and by reducing ROS production through activation of the Nrf2 pathway. Although further studies are needed to inquire its efficacy in vivo, FST appears to have potential use as an adjunctive or as a prophylactic treatment for osteoclastic bone disease.

scholarly journals Low-Level Laser Irradiation Stimulates RANKL-Induced Osteoclastogenesis via the MAPK Pathway in RAW 264.7 Cells

2021 ◽  
Vol 11 (12) ◽  
pp. 5360
Author(s):  
Jae-Min Song ◽  
Bong-Soo Park ◽  
Sang-Hun Shin ◽  
In-Ryoung Kim
Keyword(s):  
Laser Irradiation ◽  
Osteoclast Differentiation ◽  
Bone Diseases ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Metabolic Bone Diseases ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser ◽  
Low Level Laser Irradiation

Low-level laser therapy (LLLT) is recognized as an effective medical tool for the treatment of various conditions requiring tissue repair, pain relief, inflammation treatment, and restoration of tissue dysfunction, and its development and research are growing rapidly. However, studies that analyze molecular biology by applying LLLT to osteoclasts are still insufficient to understand the mechanism. In order for LLLT to be suggested as an appropriate treatment method for the treatment of various bone diseases, it is necessary to elucidate the effect and mechanism of LLLT on osteoclast differentiation. In this study, we investigated the effect of LLLT on osteoclast differentiation using murine macrophage (RAW 264.7) cells by means of a Ga-As-Al laser (λ = 810, 80 mW). Our results indicate that LLLT did not induce cytotoxicity in RAW 264.7 cells. When LLLT was applied for 15 s to osteoclasts exposed to RANKL, the expression of NF-κB, ERK, p38, and c-Fos, which are associated with expression of NFATc1, was increased. The RT-PCR results also demonstrated significantly increased expression of osteoclast-specific genes, including NFATc1, TRAP, the calcitonin receptor, and cathepsin K, compared with the control. Taken together, we concluded that low-level laser irradiation induces osteoclastogenesis by enhancing the expression of NF-κB, MAPKs (ERK, p38), c-Fos, and NFATc1 in RAW 264.7 cells. These findings indicate that low-level laser irradiation could be considered a potential treatment option in various metabolic bone diseases that require osteoclastic activity and bone formation.

scholarly journals Protective Effects of Fermented Oyster Extract against RANKL-Induced Osteoclastogenesis through Scavenging ROS Generation in RAW 264.7 Cells

2019 ◽  
Vol 20 (6) ◽  
pp. 1439 ◽  
Author(s):  
Jin-Woo Jeong ◽  
Sung Choi ◽  
Min Han ◽  
Gi-Young Kim ◽  
Cheol Park ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Osteoclast Differentiation ◽  
Bone Diseases ◽  
Raw 264.7 Cells ◽  
Ros Generation ◽  
Tartrate Resistant Acid Phosphatase ◽  
Raw 264.7 ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Induced Expression

Excessive bone resorption by osteoclasts causes bone loss-related diseases and reactive oxygen species (ROS) act as second messengers in intercellular signaling pathways during osteoclast differentiation. In this study, we explored the protective effects of fermented oyster extract (FO) against receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclast differentiation in murine monocyte/macrophage RAW 264.7 cells. Our results showed that FO markedly inhibited RANKL-induced activation of tartrate-resistant acid phosphatase and formation of F-actin ring structure. Mechanistically, FO has been shown to down-regulate RANKL-induced expression of osteoclast-specific markers by blocking the nuclear translocation of NF-κB and the transcriptional activation of nuclear factor of activated T cells c1 (NFATc1) and c-Fos. Furthermore, FO markedly diminished ROS production by RANKL stimulation, which was associated with blocking the expression of nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1) and its regulatory subunit Rac-1. However, a small interfering RNA (siRNA) targeting NOX1 suppressed RANKL-induced expression of osteoclast-specific markers and production of ROS and attenuated osteoclast differentiation as in the FO treatment group. Collectively, our findings suggest that FO has anti-osteoclastogenic potential by inactivating the NF-κB-mediated NFATc1 and c-Fos signaling pathways and inhibiting ROS generation, followed by suppression of osteoclast-specific genes. Although further studies are needed to demonstrate efficacy in in vivo animal models, FO may be used as an effective alternative agent for the prevention and treatment of osteoclastogenic bone diseases.

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