Network Pharmacology-Based Strategy to Investigate the Mechanisms of in Treating Osteoarthritis.

is a representative tonifying kidney drug and is widely used for osteoarthritis (OA) in traditional Chinese medicine. However, its regulatory mechanisms in treating OA remain to be sufficiently investigated. The main chemical components of were screened through the TCMID database and the corresponding targets were acquired through SwissTargetPrediction. The OA-related targets were obtained from the OMIM, Genecards, Genebank, TTD, and DisGeNET databases. The prediction of key targets and pathways of in the treatment of OA was achieved by constructing a compounds-targets network and performing KEGG enrichment analysis. The OA model rats were established by the Hulth method and used to explore the protective effect of via cartilage pathological assessment. In vitro models of OA were built by the proinflammatory factor interleukin-1 (IL-1) induced SW1353 cells and used to validate the mechanisms predicted by network pharmacology. Network pharmacology results suggested that the therapeutic effects of were closely related to matrix metalloproteinase (MMP)-1, 3, 13 and inflammation-related gene COX2, which are regulated by the NFB pathway. In vivo experiments revealed that could effectively restrain cartilage from degeneration and inhibit the mRNA expression of MMP-1, MMP-3, MMP-13, and COX2 in cartilage. In vitro experiments indicated that water extract (CBWE) could significantly inhibit the expression of MMP-1, MMP-3, MMP-13, and PGE in IL-1-induced SW1353 cells and markedly prevent the translocation of NFB p65 from the cytoplasm to the nuclei and decrease its phosphorylation level. After small-interfering RNA (siRNA) was used to suppress the synthesis of NFB p65 to block NFB signaling pathway, the ability of CBWE to inhibit MMP-1, MMP-3, MMP-13, and PGE was greatly reduced. has a chondroprotective effect on OA by inhibiting the response to inflammation and substrate degradation, and the related mechanism is associated with the inhibition of the NFB pathway.