Department of Orthopedics, Fuzhou Second Hospital Affiliated to Xiamen University, Fuzhou, Fujian, China.
Biosci Biotechnol Biochem. 2021 Feb 18;85(2):332-339. doi: 10.1093/bbb/zbaa010.
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.
山柰酚苷具有促成骨作用，可防止骨质流失。然而，山柰酚苷调节骨形成的详细机制尚不清楚。山柰酚苷可以通过促进 PI3K/Akt/mTOR 信号通路来维持细胞内稳态。本研究旨在探讨 PI3K/Akt/mTOR 信号通路在山柰酚苷调节成骨中的意义。结果表明，山柰酚苷可促进成骨前体细胞 MC3T3-E1 中 PI3K、Akt 和 mTOR 的活性。山柰酚苷促进 MC3T3-E1 向成熟成骨细胞分化的作用可被 PI3K 或 mTOR 的药理学抑制剂逆转。重要的是，在山柰酚苷存在的情况下，PI3K 抑制剂抑制的成骨细胞分化可被 mTOR 过表达逆转。体内实验表明，在去卵巢小鼠的骨组织中，PI3K 或 mTOR 的药理学抑制剂可逆转山柰酚苷增强的成骨作用。总之，山柰酚苷可通过 PI3K/Akt/mTOR 信号通路促进成骨作用，为山柰酚苷治疗骨质疏松症的策略提供了新线索。
