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Morroniside promotes the osteogenesis by activating PI3K/Akt/mTOR signaling
Morroniside exerts a proosteogenic effect, which can prevent bone loss. However, the detailed mechanism underlying Morroniside-regulated bone formation is unclear. Morroniside can maintain cell homeostasis by promoting PI3K/Akt/mTOR signaling. The purpose of this study is to explore the significance...
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Published in: | Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2021-02, Vol.85 (2), p.332-339 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Morroniside exerts a proosteogenic effect, which can prevent bone loss. However, the detailed mechanism underlying Morroniside-regulated bone formation is unclear. Morroniside can maintain cell homeostasis by promoting PI3K/Akt/mTOR signaling. The purpose of this study is to explore the significance of PI3K/Akt/mTOR signaling in Morroniside-regulated osteogenesis. The results showed that Morroniside promoted the activities of PI3K, Akt, and mTOR in osteoblast precursor MC3T3-E1. The differentiation of MC3T3-E1 to mature osteoblasts promoted by Morroniside can be reversed by the pharmacological inhibition of PI3K or mTOR. Importantly, in the presence of Morroniside, the osteoblast differentiation suppressed by PI3K inhibitor was reversed by mTOR overexpression. In vivo assays showed that in bone tissue of ovariectomized mice, Morroniside-enhanced osteoblast formation was reversed by the pharmacological inhibition of PI3K or mTOR. In conclusion, Morroniside can promote the osteogenesis through PI3K/Akt/mTOR signaling, which provides a novel clue for the strategy of Morroniside in treating osteoporosis. |
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ISSN: | 1347-6947 1347-6947 |
DOI: | 10.1093/bbb/zbaa010 |