Abstract
In this study, we employed network pharmacology and molecular docking techniques, complemented by experimental validation, to assess the pharmacodynamic effects of tenghuang jiangu wan (THJGW) in the context of osteoporosis (OP) treatment. Our investigation delineated the underlying mechanism of action. To simulate clinical postmenopausal osteoporosis, we used a rat model of bilateral ovary removal. Through assessment of bone mineral density, bone microstructure, histological examination of bone tissues and evaluation of biochemical markers, it was confirmed that THJGW can effectively increase the number of bone trabeculae in ovx rats and improve structural damage. In addition, it has a significant protective effect on bone turnover, thereby demonstrating its therapeutic potential for OP. Furthermore, using bioinformatics analysis, we predicted that THJGW could modulate various processes in vivo. These include the regulation of inflammatory responses, growth factors, steroid hormone levels, biosynthetic pathways, and effects on lipids and atherosclerosis. Additionally, we investigated its role in the lipid and atherosclerosis signaling pathway. By activating the Wnt/β-catenin signaling pathway and concurrently inhibiting the Axin2/PPAR-γ signaling pathway, THJGW promotes the proliferation and differentiation of bone marrow mesenchymal stem cells into osteoblasts, reduces adipocyte production, and enhances bone formation. This dual mechanism underscores their preventive and therapeutic potential against OP. This study provides valuable scientific insights and a robust theoretical foundation for the clinical use of THJGW.
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