裸花紫珠调节巨噬细胞治疗反复性骨骼肌损伤OA

Aim To investigate the mechanism by which Callicarpa nudiflora Hook.ex Arn.(CN)regu-lates macrophages to promote repair following recur-rent skeletal muscle injury.Methods Rats were di-vided into control,model,and treatment groups.Re-current tibialis anterior muscle injury was induced in the model and treatment groups,with the treatment group receiving treatment via gavage.Tissue samples were collected at multiple time points,and repair pro-cesses and mechanisms were evaluated using histol-ogy,UPLC-HRMS,network pharmacology,and pro-tein detection.Macrophages treated with CN-containing serum were assessed for proliferation/migra-tion and JAK/STAT pathway activity.Results CN promoted early myogenic repair and reduced fibrosis.Network pharmacology revealed that core targets were enriched in cytokine-receptor interactions,JAK-STAT,and NF-κB signaling pathways.CN increased macrophage infiltration in injured muscle,enhanced macrophage proliferation and migration,and upregu-lated IL-6 and TNF-α levels during the acute phase.CN activated the JAK1/STAT3 signaling pathway in macrophages,promoted the release of inflammatory factors,upregulated the NF-κB signaling pathway,and stimulated satellite cell proliferation.Conclu-sions CN activates the JAK1/STAT3 axis in macro-phages,promotes the release of acute-phase inflamma-tory factors and NF-κB signaling pathway activation,and thereby enhances early repair of recurrent skeletal muscle injury.