Isovitexin can Alleviate Fracture-Related Infection, Promote Osteogenesis, and Inhibit Activation of the NF-κB Signaling Pathway

Fracture-related infection is a challenging aspect of orthopedic care, as it leads to prolonged inflammation and impaired bone healing. Although isovitexin is a naturally occurring flavonoid with anti-inflammatory properties, its effects on fracture-related infection remain unclear. A rat fracture infection model was established and randomly divided into four groups: control, model, Vancomycin, and isovitexin. Tissue staining was used to assess bone healing. In contrast, enzyme-linked immunosorbent assay and biochemical kits were used to measure the levels of inflammatory factors and bone metabolism-related indicators. The expression of proteins associated with osteogenesis and the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway was examined using Western blot. When compared to the model group, isovitexin treatment more effectively reduced inflammatory cell infiltration in bone tissue and promoted callus formation than the Vancomycin group. In addition, isovitexin improved the imbalance of bone metabolism and promoted the expression of osteogenesis-related proteins Bone Morphogenetic Protein 2 (BMP2), Osteopontin (OPN), and Runt-related Transcription Factor 2 (RUNX2). It also decreased the levels of pro-inflammatory factors tumor necrosis factor (TNF)-α and interleukin (IL)-6, and increased the level of the anti-inflammatory factor IL-10. Mechanistic studies showed that isovitexin significantly inhibited the activation of the NF-κB signaling pathway. Isovitexin can promote bone metabolism and healing, suppress the NF-κB signaling pathway, and reduce the inflammatory response associated with fracture-related infection. This study suggests that isovitexin may be a viable therapy option for fracture-related infections.