Effect of geniposide on periodontal inflammation and gingival angiogenesis in rats by regulating the IKK/NF-κB pathway

Objective To investigate the effects of geniposide on periodontal inflammation and gingival angiogenesis, and to preliminarily explore its mechanism of action based on the IKK/NF-κB signaling pathway.

Methods A rat model of experimental periodontitis was established using the ligation method.Forty successfully modeled rats were randomly divided into a model group and low, medium, high geniposide groups, with 10 rats in each group.The rats in the low, medium, high geniposide groups were administered 5, 10, 20 mg/kg geniposide via gavage, respectively.An additional 10 rats were selected as the control group and did not undergo modeling.Micro-CT imaging was used to evaluate alveolar bone resorption, bone mineral density (BMD), and bone volume/tissue volume (BV/TV) in each group.Western blotting and immunohistochemistry were employed to analyze histopathological damage and expression of related proteins in each group.

Results Compared with the control group, the model group exhibited decreased BMD and BV/TV, while the alveolar bone resorption and protein expression of TNF-α, IL-1β, PECAM, VEGF, p-IKKα, p-IKKβ, p-IκB, and p-NF-κB p65 in gingival tissues were significantly increased (P < 0.05).Compared with the model group, the low, medium, and high dose geniposide groups showed increased BMD and BV/TV, along with reduced alveolar bone resorption and decreased expression of TNF-α, IL-1β, PECAM, VEGF, p-IKKα, p-IKKβ, p-IκB, and p-NF-κB p65 in gingival tissues (P < 0.05).

Conclusions Geniposide facilitates the repair of alveolar bone loss and inhibits the periodontal inflammatory response in rats with periodontitis, the mechanism of which may be associated with the suppression of IKK/NF-κB signaling pathway.