Magnolol prevents ossified tendinopathy by inhibiting PGE2-induced osteogenic differentiation of TDSCs
International Immunopharmacology, ISSN: 1567-5769, Vol: 70, Page: 117-124
2019
- 11Citations
- 30Captures
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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.
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Metrics Details
- Citations11
- Citation Indexes11
- 11
- CrossRef10
- Captures30
- Readers30
- 30
Article Description
Magnolol is a compound that is extracted from magnolia, is used in Chinese medicine and is a type of lignan. Magnolol has various anti-inflammation, anti-proliferation and pro-autophagy effects. Ossified tendinopathy affects many athletes and people with repetitive tendon injuries. Ossified tendinopathy is a tremendous economic burden, and no effective and safe drugs are available to prevent the pathogenesis of ectopic ossification. In this study, we aimed to study how magnolol affects ossified tendinopathy by evaluating its effects on osteogenic differentiation of tendon-derived stem cells (TDSCs). Our data suggested that magnolol attenuated ectopic ossification in the Achilles tendon caused by Achilles tenotomy. Magnolol inhibited PGE2-induced ALP activity and prevented calcium deposits in TDSCs in vitro. Magnolol also exerted inhibitory effects on expression of osteogenic factors, such as Runx2, OCN, and BMP2 in vivo. Further investigation revealed the underlying mechanism by which magnolol prevents PGE2-induced ectopic ossification. Specifically, magnolol inhibits PGE2-induced PI3K/AKT/β-catenin pathway activation in TDSCs. Our findings demonstrated that magnolol inhibited ossified tendinopathy through preventing osteogenic differentiation of TDSCs via downregulation PGE2-induced PI3K/AKT/β-catenin pathways.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S156757691930284X; http://dx.doi.org/10.1016/j.intimp.2019.02.010; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85061821473&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/30798160; https://linkinghub.elsevier.com/retrieve/pii/S156757691930284X; https://dx.doi.org/10.1016/j.intimp.2019.02.010
Elsevier BV
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