Plumbagin Attenuates Periodontitis by Inhibiting the PI3K/AKT Pathway and Enhancing Autophagy: A Potential Therapeutic Strategy

Abstract

Background and Purpose Plumbagin (PLB), a natural compound derived from Plumbago zeylanica L., exhibits potent antioxidant, anti-inflammatory, antibacterial, and anticancer properties. However, its role in modulating periodontitis via the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway and autophagy remains unclear. This study explores PLB’s therapeutic potential in periodontitis, focusing on these mechanisms. Materials and Methods In vitro , Cell Counting Kit-8 was used to examine cell viability, and LysoTracker Red was used to assess the degree of autophagy activation. The effects of PLB on periodontitis and the PI3K/AKT signaling pathway in vitro were detected by real-time quantitative polymerase chain reaction and Western blot. In vivo , we established rat models of periodontitis to validate the efficacy of PLB. Results PLB exhibited a dose-related suppressive influence on periodontitis progression. Notably, PLB significantly downregulated the components of the PI3K/AKT pathway and modulated autophagy. In rat models, PLB treatment effectively alleviated periodontal inflammation and alveolar bone resorption. Conclusion PLB exhibits anti-inflammatory properties in periodontitis by suppressing the PI3K/AKT pathway and enhancing autophagy. Our results offer a scientific basis for using PLB in the treatment of periodontitis, emphasizing its promise as an innovative remedy for this dental condition.