ArticleInternational journal of molecular sciences2025
Mechanistic Integration of Network Pharmacology and In Vivo Validation: TFRD Combat Osteoporosis via PI3K/AKT Pathway Activation.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mechanotransduction Failure and Molecular Rescue in Gastric Cancer: Kinetotherapy Across the IL-6/STAT3-Myostatin/ACVR2B-Akt/mTOR Axis.Medical sciences (Basel, Switzerland) · 2026Review
- Huoxue Jiegu compound capsule accelerates tibial fracture healing via angiogenesis-driven repair mechanisms.Frontiers in medicine · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
In the context of osteoporosis closely linked to bone metabolism imbalance caused by estrogen deficiency, total flavonoids of Rhizoma Drynariae (TFRD) exhibit potential anti-osteoporotic activity, yet their multicomponent synergistic mechanism and association with the PI3K/AKT signaling pathway remain unclear. This study aimed to systematically elucidate the molecular mechanisms by which TFRD regulate bone metabolism and improve osteoporosis in ovariectomized (OVX) rats through the PI3K/AKT pathway, integrating network pharmacological predictions with animal experimental validation. Methods involved identifying TFRD's active components using UPLC/MS-MS, predicting targets with SwissTargetPrediction, constructing a "component-target-disease" network, and performing GO/KEGG enrichment analysis with MetaScape (v3.5). In vivo experiments established an OVX rat model, randomized into sham, OVX, low-/high-dose TFRD, and sim groups, assessing bone mineral density (BMD) and mandibular Micro-CT parameters after 12 weeks. Western blot analyzed PI3K, p-AKT1, and related protein expressions. Results showed the high-dose TFRD group significantly increased BMD, improved trabecular bone quantity and structure, and upregulated PI3K, p-PI3K, and p-AKT1 protein expressions compared to the OVX group. Molecular docking confirmed stable binding energy between core components and PI3K/AKT targets. TFRD may ameliorate estrogen deficiency-induced osteoporosis by activating the PI3K/AKT signaling pathway, inhibiting bone resorption, and promoting osteogenic differentiation, providing pharmacological evidence for multitarget treatment of osteoporosis with traditional Chinese medicine.
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