&lt;i&gt;Sargassum serratifolium&lt;/i&gt; attenuates RANKL-induced osteoclast differentiation and oxidative stress through inhibition of NF-κB and activation of the Nrf2/HO-1 signaling pathway

Kim, Hong Jae; Park, Cheol; Kim, Gi‐Young; Park, Eui Kyun; Jeon, You‐Jin; Kim, Suhkmann; Hwang, Hye Jin; Choi, Yung Hyun

doi:10.5582/bst.2018.01107

Cited by 18 publications

(9 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To investigate the inhibitory effect of FO on the formation of F-actin rings in mature osteoclasts, cells cultured under the same conditions as in the differentiation inhibition assay were fixed at room temperature for 10 min by replacing the culture medium with 4% paraformaldehyde solution, as previously described [53]. The cells were washed with ice-cold PBS and then stained with fluorescein isothiocyanate (FITC)-phalloidin solution (Thermo Scientific, Waltham, MA, USA) in darkness for 45 min following a 5 min treatment with a 0.1% Triton X-100 solution to permeabilize the cells.…”

Section: Methodsmentioning

confidence: 99%

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

Jeong

Choi

Han

et al. 2019

IJMS

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Methodsmentioning

confidence: 99%

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

Jeong

Choi

Han

et al. 2019

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…The cells were cultured in DMEM containing 10% heat inactivated FBS, penicillin (100 units/mL) and streptomycin (100 g/mL) at 37 °C in a humidified 5% CO 2 atmosphere and subcultured every 3 days. The viability of the cells was assessed by MTT assay as previously described [14]. Briefly, the cells were treated with the desired concentrations of FST with or without 100 ng/mL RANKL for 72 h and then incubated with 50 μg/mL MTT solution for 3 h. Formazan crystals were dissolved in DMSO and the absorbance was measured using an enzyme-linked immunosorbent assay (ELISA) microplate reader (Dynatech Laboratories, Chantilly, VA, USA) at 540 nm.…”

Section: Methodsmentioning

confidence: 99%

“…As described previously, evaluation of actin ring formation was performed [14]. Briefly, the cells were fixed with 4% paraformaldehyde, permeabilized with 0.1% Triton X-100 in PBS for 5 min and then stained with an anti-actin antibody at 4 °C overnight.…”

Section: Methodsmentioning

confidence: 99%

“…As described previously, total protein was extracted from the cells using the Bradford Protein assay kit [14]. Nuclear and cytosolic proteins were prepared using a NE-PER nuclear and cytoplasmic extraction reagents kit according to the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

“…The binding of RANKL to its receptor RANK results in the activation of various signaling pathways, including the NF-κB pathway [6,7], which then enhances the activation of nuclear factor of activated T cell c1 (NFATc1), which then in turn promotes osteoclast formation by up-regulating the expression of osteoclast-specific genes [8,9]. In addition, a number of previous studies have shown that reactive oxygen species (ROS) are also critical messengers for osteoclast differentiation [10,11] and increased activity of the Nrf2 signaling system can block this activation [12,13,14]. These findings suggest that suppression of ROS production in combination with increasing activity of Nrf2 may provide a means to block osteoclast activity.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Jeong

Lee

et al. 2019

Foods

View full text Add to dashboard Cite

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.

show abstract

Rubiadin Regulates Bone Metabolism in Ovariectomized Rat Model by Inhibition of osteoclast formation and differentiation

et al. 2023

View full text Add to dashboard Cite

The present study investigated the effect of rubiadin from morinda officinalis on bone metabolism in an ovariectomized rat model. Results from the MTT test showed that the best drug concentration was 0.6 mg for 24 h (P>0.05). Compared with the Control group, the femoral bone mineral density in the experimental group treated with rubiadin was significantly higher (P<0.05). After the intervention of rubiadin, the level of P1NP in serum increased, the level of β‐CTX decreased, and the level of estradiol increased. The up‐regulated genes C−C motif chemokine ligand 2 (CCL2), Inhibitor of Nuclear Factor Kappa B Kinase Subunit Beta (IKBKB), C1q, C6, Suppressor of cytokine signaling1 (SOCS1/3) and Dickkopf‐3 (DKK3) were screened from the data. Down regulated genes wnt6, Sfrp5, COL4A6, Ig like R. The differential genes were detected by RT‐PCR. Compared with the Control group, CCL2 and SOCS3 were significantly up‐regulated in the experimental group (P<0.05), and COL4A6 and LILRB3a were significantly down regulated in the experimental group (P<0.05). Western blot test results showed that the expression of LILRB3a protein was significantly reduced, while the expression of SOCS3 protein was significantly increased, indicating that rubiadin could significantly increase the expression of SOCS3 protein and reduce the expression of LILRB3a protein. In conclusion, rubiadin inhibits the formation and differentiation of osteoclasts by affecting the expression of CCL2 and SOCS3, COL4A6 and LILRB3a genes. Therefore, rubiadin can be of therapeutic importance for the treatment of osteoporosis.

show abstract

<i>Sargassum serratifolium</i> attenuates RANKL-induced osteoclast differentiation and oxidative stress through inhibition of NF-κB and activation of the Nrf2/HO-1 signaling pathway

Cited by 18 publications

References 46 publications

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

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

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

Rubiadin Regulates Bone Metabolism in Ovariectomized Rat Model by Inhibition of osteoclast formation and differentiation

Contact Info

Product

Resources

About