Background: Rosa roxburghii Tratt. (Cili), a medicinal-edible herb predominantly distributed in Guizhou Province, exhibits diverse pharmacological properties, including anti-inflammatory, antioxidant, and cell proliferation-promoting effects. Despite its recognized pharmacological value, the therapeutic efficacy and underlying mechanisms in fracture healing remain unexplored. This study aims to systematically investigate its potential mechanisms by integrating network pharmacology and molecular docking. Methods: The components of R. roxburghii Tratt. were retrieved from the PubChem, CNKI, VIP, and WANFANG databases, and their corresponding targets were screened from public databases. The targets of fracture healing were obtained from the GeneCards and OMIM databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed the mechanisms of R. roxburghii Tratt. in fracture healing. The potential targets and core components were identified by constructing a protein-protein interaction network and a series of topological networks. Finally, molecular docking was performed to validate the binding of the core targets to the components. Results: Gene Ontology analysis highlighted its regulation of vascular endothelial growth factor signaling pathway, cell migration, epidermal growth factor receptor signaling pathways, and fibroblast growth factor receptor signaling pathways. Kyoto Encyclopedia of Genes and Genomes analysis suggested that R. roxburghii Tratt.’s mechanism may involve key pathways, such as hypoxia-inducible factor 1, phosphoinositide 3-kinase/protein kinase B, mitogen-activated protein kinase, tumor necrosis factor, and ras-associated protein-1 signaling pathway, while topological network analysis identified 4 core targets (tumor necrosis factor, prostaglandin G/H synthase 2, epidermal growth factor receptor, and proto-oncogene tyrosine-protein kinase Src) and 21 core components (naringenin, quercetin, kaempferol, isorhamnetin, luteolin, myricetin, etc), all critically associated with osteogenesis and angiogenesis. Molecular docking confirmed strong binding between these components and targets. Conclusion: These findings propose that R. roxburghii Tratt. may accelerate fracture healing by multitarget, components, and pathways regulating osteogenesis and angiogenesis, providing a scientific basis for its development and utilization.

Background: Breast cancer is a highly common malignancy in women, with bone as its most frequent site of distant metastasis significantly increasing mortality risk. Methods: This study integrated single‐cell RNA sequencing datasets (GSE266330 and GSE243526) to systematically characterize the tumor microenvironment across normal tissue, primary tumor, and bone metastasis in breast cancer. Results: In total, 141 056 high‐quality single cells were analyzed from an integrated cohort comprising a bone‐metastasis dataset (GSE266330) and a primary/normal breast dataset (GSE243526), identifying 11 major cell types. Within the bone‐metastatic cohort, we identified a macrophage subpopulation highly expressing SPP1 (Mac‐SPP1) that exhibited an M2‐polarized signature and elevated metabolic gene‐set enrichment, and that expressed transcription factors such as HOXA9 and MAF. We also identified CD4‐S100A9 and CD8‐GZMK T‐cell subpopulations with high cytotoxicity, high exhaustion, and metabolic reprogramming. Pseudotime analysis positioned CD4‐S100A9 cells at one end of the inferred CD4+ T‐cell trajectory and CD8‐GZMK cells at an intermediate node along the inferred CD8+ T‐cell trajectory. Cell–cell communication analysis predicted that Mac‐SPP1 interacts with these T‐cell subsets through the SPP1‐integrin (e.g., SPP1‐CD44) and CD74‐MIF/COPA signaling axes. Conclusion: This study provides a single‐cell characterization of the breast cancer bone‐metastatic microenvironment, identifying an SPP1‐expressing macrophage subset (Mac‐SPP1) and predicting its interactions with CD4‐S100A9 and CD8‐GZMK T cells. Because the bone‐metastatic and primary/normal specimens derive from different datasets, these findings are descriptive and cannot be attributed to metastatic progression alone and require experimental validation and confirmation in cohorts that profile primary and metastatic specimens within a single study.

Dendrobium has long been used in traditional medicine to manage liver disorders. Dendrobine is a major alkaloid compound isolated from Dendrobium that has demonstrated promising hepatoprotective activity in preliminary pharmacological studies, but the molecular mechanisms through which it functions remain insufficiently defined. Here, we elucidated the potential mechanisms by which dendrobine mitigates liver injury using an integrative approach that combines network pharmacology with molecular docking. Putative dendrobine-associated targets relevant to liver injury were first predicted through network pharmacology analyses. A protein-protein interaction (PPI) network was subsequently constructed to identify central therapeutic targets. Molecular docking was then applied to validate the interactions between dendrobine and key proteins. Ten core targets were ultimately identified (NR1H4, ESR1, KDR, NOS3, GSK3B, IL-2, CASP3, PRKACA, PPARA and PPARG), and dendrobine showed strong predicted affinity for these proteins. These findings indicate that dendrobine may exert hepatoprotective effects by modulating these central molecular targets and associated signaling proteins. Overall, this work provides a systematic framework for delineating the pharmacological actions and potential protein targets of natural bioactive compounds.