Chinese Journal of Tissue Engineering Research ›› 2026, Vol. 30 ›› Issue (28): 7237-7244.doi: 10.12307/2026.680

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Function and molecular mechanism of physcion in regulating bone homeostasis

Qi Yuxin1, 2, Dang Yifan1, 2, Dai Liming2, Zhang Xiaoling1, 2   

  1. 1Collaborative Innovation Center of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China; 2Department of Orthopedics, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
  • Received:2025-06-26 Revised:2025-10-20 Online:2026-10-08 Published:2026-02-07
  • Contact: Zhang Xiaoling, Professor, Doctoral supervisor, Collaborative Innovation Center of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China; Department of Orthopedics, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
  • About author:Qi Yuxin, MS candidate, Collaborative Innovation Center of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
  • Supported by:
    National Natural Science Foundation of China, No. 32370892 (to ZXL)

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Abstract: BACKGROUND: Although physcion has been shown to have protective effects against osteoporosis, the exact mechanism is not fully understood.
OBJECTIVE: Through multidimensional analysis of the regulatory effect of physcion on the AKT signaling pathway, the molecular mechanism of its regulation on osteoclast induced differentiation and osteogenic function induced differentiation is revealed.
METHODS: (1) RAW264.7 cells and C3H10T1/2 cells were cultured in vitro and subsequently exposed to 0, 10, 20, 30, 40, 50, and 60 µmol/L physcion, respectively. The cytotoxicity of physcion was detected by cell counting kit-8 assay. (2) RAW264.7 cells and C3H10T1/2 cells were treated with different concentrations (0, 20, and 40 µmol/L) of physcion during osteoclast and osteogenic differentiation, respectively. The differentiation ability was detected by quantitative polymerase chain reaction, western blot assay, and alkaline phosphatase staining, respectively. (3) Based on network pharmacology, the regulation of osteoclast differentiation by physcion and related pathways was analyzed, and molecular docking was performed for target proteins. (4) Western blot assay was used to verify the regulatory effect of physcion on the phosphorylation of AKT in the AKT axis—a downstream pathway.
RESULTS AND CONCLUSION: (1) Exposure to concentrations of 0-60 µmol/L of physcion resulted in cell survival rates of over 90% in all groups, with no significant cytotoxicity observed. (2) Physcion significantly inhibited the expression of genes related to osteoclast differentiation, with Acp5, CTSK, DC-STAMP, and Nfatc1 showing a downregulation trend. However, it has no significant effect on the expression of genes related to osteoblast differentiation, COL1A1, Runx2, OSX, and alkaline phosphatase staining intensity. (3) According to network pharmacology and molecular docking, physcion affects osteoclast differentiation and regulates the PI3K-AKT pathway, with a binding energy of -10.72 kJ/mol to the AKT1 target and strong binding activity. (4) During osteoclast differentiation, the p-AKT/AKT ratio of RAW264.7 cells was increased (n=3, P=0.006 3), while physcion decreased this ratio. These findings demonstrate that physcion inhibits osteoclast differentiation by regulating the AKT signaling pathway, thereby regulating bone homeostasis. 

Key words: network pharmacology, physcion, bone homeostasis, osteoclast, osteoblast

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