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

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Article · Volume 22, Issue 3 · pp. 850–860

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

Shiya Li1, Fang Qian1, Huili Wu1, Chen Tang1, Lijuan Wang1

  1. 1Department of Endodontics, Zhonglou Branch, Changzhou Traditional Chinese Medicine Hospital, Changzhou, Jiangsu, China.

Abstract

Background and Objectives: 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.

Keywords: Periodontitis; plumbagin; autophagy; anti-inflammatory; rat model; PI3K/AKT pathway

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