# A 70% Ethanol Neorhodomela munita Extract Attenuates RANKL-Induced Osteoclast Activation and H2O2-Induced Osteoblast Apoptosis In Vitro

**Authors:** Seongtae Jeong, Il-Kwon Kim, Hanbyeol Moon, Hojin Kim, Byeong-Wook Song, Jung-Won Choi, Sang Woo Kim, Seahyoung Lee, Dong-Sik Chae, Soyeon Lim

PMC · DOI: 10.3390/molecules29081741 · Molecules · 2024-04-11

## TL;DR

This study shows that a seaweed extract can reduce bone loss by inhibiting harmful cell activity and may serve as a natural treatment for osteoporosis.

## Contribution

The study introduces Neorhodomela munita ethanol extract as a novel natural compound that modulates osteoclast and osteoblast pathways.

## Key findings

- EN inhibits RANKL-induced osteoclast formation by targeting the MAPKs-NFATc1/c-Fos pathway.
- EN reduces H2O2-induced osteoblast apoptosis through downregulation of apoptotic signals.
- EN shows potential as a natural alternative to conventional osteoporosis treatments.

## Abstract

The rapid aging of the population worldwide presents a significant social and economic challenge, particularly due to osteoporotic fractures, primarily resulting from an imbalance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. While conventional therapies offer benefits, they also present limitations and a range of adverse effects. This study explores the protective impact of Neorhodomela munita ethanol extract (EN) on osteoporosis by modulating critical pathways in osteoclastogenesis and apoptosis. Raw264.7 cells and Saos-2 cells were used for in vitro osteoclast and osteoblast models, respectively. By utilizing various in vitro methods to detect osteoclast differentiation/activation and osteoblast death, it was demonstrated that the EN’s potential to inhibit RANKL induced osteoclast formation and activation by targeting the MAPKs-NFATc1/c-Fos pathway and reducing H2O2-induced cell death through the downregulation of apoptotic signals. This study highlights the potential benefits of EN for osteoporosis and suggests that EN is a promising natural alternative to traditional treatments.

## Linked entities

- **Genes:** TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600], NFATC1 (nuclear factor of activated T cells 1) [NCBI Gene 4772], FOS (Fos proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2353]
- **Chemicals:** H2O2 (PubChem CID 784), Ethanol (PubChem CID 702)
- **Diseases:** osteoporosis (MONDO:0005298)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Nfatc1 (nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1) [NCBI Gene 18018] {aka 2210017P03Rik, NF-ATc, NFAT2, NFATc, Nfatcb}, Fos (Fos proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 14281] {aka D12Rfj1, c-fos, cFos}, Tnfsf11 (tumor necrosis factor (ligand) superfamily, member 11) [NCBI Gene 21943] {aka Ly109l, ODF, OPGL, RANKL, Trance}
- **Diseases:** osteoporosis (MESH:D010024), osteoporotic fractures (MESH:D058866)
- **Chemicals:** EN (-), H2O2 (MESH:D006861)
- **Cell lines:** Saos-2 — Homo sapiens (Human), Osteosarcoma, Cancer cell line (CVCL_0548), Raw264.7 — Mus musculus (Mouse), Mouse leukemia, Cancer cell line (CVCL_0493)

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11052068/full.md

## References

55 references — full list in the complete paper: https://tomesphere.com/paper/PMC11052068/full.md

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Source: https://tomesphere.com/paper/PMC11052068