| Objective To reveal the potential mechanism of Bushen Yijing Formula in treating type 2 diabetic osteoporosis (T2DOP) by using network pharmacology and animal experiments. Methods The active components and targets of the compound were screened through platforms such as TCMSP and HERB, and then cross-referenced with disease genes obtained from OMIM, GeneCards, and PharmGkb to obtain 225 intersection targets. The "drug-component-target" and PPI networks were constructed using Cytoscape and STRING, and GO/KEGG enrichment was completed by David. Molecular docking was performed using AutoDock Vina. Subsequently, a T2DOP rat model was established, and blood glucose metabolism indicators were measured. Western blot and IHC were used to detect the expression of SRC, TP53, and AKT1 in bone tissue. Results SRC, TP53, and AKT1 were the core targets of the network; there were 1,205 GO entries and 177 KEGG pathways. Molecular docking showed that linoleic acid and poricoic acid C had strong affinity for key proteins. In vivo experiments indicated that the formula could reduce blood glucose and β-CTX, increase insulin, and the high-dose effect was better. At the same time, it downregulated SRC and TP53 and upregulated AKT1, inhibiting bone resorption and promoting bone formation. Conclusion BushenYijing Formula improves glucose and bone metabolism through a "multi-component-multi-target-multi-pathway" mode, and its effect is closely related to the regulation of SRC, TP53, and AKT1, providing a new basis for the prevention and treatment of T2DOP. |