ArticleJournal of inflammation research2026
Hydroxygenkwanin Identified in Rehmanniae Radix Praeparata-Corni Fructus Ameliorates Postmenopausal Osteoporosis via Modulation of the AGE-RAGE Signaling Pathway.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Osteoporosis (OP) is a metabolic bone disease marked by reduced bone mass and compromised microarchitecture, increasing fragility fracture risk. The traditional Chinese herbal pair Methods: Network pharmacology, UHPLC-HRMS, molecular docking, and molecular dynamics simulations were integrated to identify the potential active components of RRP-CF and to predict the potential targets and related signaling pathways underlying its anti-osteoporotic effects. These predictions were further validated through in vitro (using 25 and 50 µM hydroxygenkwanin (HGK)) and in vivo experiments in ovariectomized (OVX) rats (using 10 and 20 mg/kg HGK). Results: UHPLC-HRMS identified HGK as one of the detectable components of RRP-CF. A total of 66 common targets between RRP-CF and OP were screened out by network pharmacology; Protein-Protein Interaction (PPI) network analysis showed that estrogen receptor 1 (ESR1), tumor protein p53 (TP53), tumor necrosis factor (TNF), signal transducer and activator of transcription 3 (STAT3), and prostaglandin-endoperoxide synthase 2 (PTGS2) were the key targets. Gene Ontology enrichment suggested that RRP-CF-associated targets were mainly involved in inflammatory response, and the advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) signaling pathway was identified as a critical pathway. In vivo experiments confirmed that RRP-CF could improve bone microstructure and collagen content, as evidenced by increased BMD (from 106.58 ± 11.09 mg/cm Conclusion: Our findings indicate that RRP-CF can inhibit bone loss in OVX rats, and suggest that HGK, as a potential active constituent of RRP-CF, may exert anti-osteoporotic effects through modulation of the AGE-RAGE pathway and downregulation of osteoclast-related proteins including p53, p-AKT, NFATc1 and CTSK. These findings provide a preliminary mechanistic basis for developing novel OP therapeutic regimens, though further pharmacokinetic and safety studies are warranted.
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