Ginsenosiderb1 Induces Apical Periodontitis Regression Via Regulating Macrophage Efferocytosis

Investigate the role and mechanism of Ginsenoside Rb1 (GRb1) in promoting regression of apical periodontitis. ① 50 SD male rats, aged from 6-8 weeks, were purchased. Animal experiments were approved by the laboratory animal Ethics Committee of the School of Medicine, Xi’an Jiaotong University. ② Establish rat AP model and feed GRb1 orally. Use Micro-ct, HE, Masson staining, and immunohistochemical staining to assess GRb1′s effect on AP and expression of related proteins in periapical tissues. ③ Develop PPAR-γ over-expressed or suppressed macrophages, treat with GRb1, and co-culture with apoptotic neutrophils. Use flow-cytometry, western blotting, and immunofluorescence staining to evaluate macrophage efferocytosis, mitochondrial fission, and inflammatory status. ④ Establish rat AP model by exposing pulp cavity of mandibular first molars. Treat with GRb1, Ca(OH)2, and GRb1+PPAR-γ inhibitor, followed by resin filling. After 4 weeks, collect mandibles for Micro-ct, HE, Masson staining, and IHC, IF staining to assess therapeutic impact and identify PPAR-γ axis regulated mitochondrial fission and macrophage efferocytosis in periapical lesions. In vivo experiments show GRb1 suppresses AP development via PPAR-γ axis regulated mitochondrial fission and macrophage efferocytosis. GRb1 promotes AP regression. In vitro studies show GRb1 enhances mitochondrial fission related protein expression and macrophage efferocytosis via PPAR-γ signaling pathway. GRb1 facilitates regression of apical periodontitis by enhancing macrophage efferocytosis capacity. Further research on GRb1 as an adjunctive treatment for apical periodontitis is recommended.