Toosendanin inhibits osteoclast formation and alleviate postmenopausal osteoporosis by regulating the p38 signaling pathway
International Immunopharmacology, ISSN: 1567-5769, Vol: 116, Page: 109745
2023
- 9Citations
- 5Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations9
- Citation Indexes9
- CrossRef7
- Captures5
- Readers5
Article Description
Disruption of the balance between osteoclasts and osteoblasts could lead to bone diseases including osteoporosis. It’s well known that RANKL-RANK signaling plays a vital role in activating osteoclasts. Herein, we explored the therapeutic effects of toosendanin (TSN) in osteoporosis, showing that TSN attenuated RANKL-stimulated osteoclastogenesis and osteoclast-specific gene expression in vitro. Bioinformatics predicted that TSN could interfere p38 subunits and regulate the MAPK cascade, and we further verified and demonstrated that TSN significantly inhibited RANKL-induced p38 signaling through western blot. In ovariectomized mouse model, TSN effectively inhibited the formation of TRAP-positive osteoclasts and exhibited protective effect against bone loss. Altogether, these data indicate that TSN targeted p38 activation to inhibit osteoclastogenesis, suggesting the possible therapeutic use of TSN in osteoporosis in the future.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1567576923000681; http://dx.doi.org/10.1016/j.intimp.2023.109745; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85146930924&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36702075; https://linkinghub.elsevier.com/retrieve/pii/S1567576923000681; https://dx.doi.org/10.1016/j.intimp.2023.109745
Elsevier BV
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