Work

Unraveling the multitarget mechanisms of aloe emodin against periodontitis: a synergy of network pharmacology and experimental validation

Year: 2026

Type: article

Abstract: Background Chronic periodontitis is a prevalent inflammatory disease that leads to destruction of periodontal tissues, resulting in tooth loss. While mechanical debridement and adjunctive antibiotics are commonly used, their therapeutic efficacy is limited by anatomical complexity and concerns over antibiotic resistance and side effects. Aloe-emodin (AE), a naturally occurring anthraquinone compound, exhibits significant anti-inflammatory and antimicrobial effects. However, its mechanisms in periodontitis remain unclear. Methods A network pharmacology approach was employed to identify potential targets of AE in periodontitis. The effects of AE on the viability, proliferation, migration, osteogenic differentiation, and inflammatory responses of mouse periodontal ligament stem cells (mPDLSCs) were assessed CCK8, qPCR and ELISA. In vivo , the alveolar bone of mouse periodontitis model was repaired and evaluated by micro-CT and histological analysis. Results Network pharmacology analysis identified 179 overlapping targets between AE and periodontitis, with key hubs including TNF, AKT1, EGFR, TP53, and MMP9. These targets were predominantly enriched in the MAPK, PI3K-AKT, NF-κB, and TNF signaling pathways. In vitro , AE significantly enhanced the proliferation, migration, and osteogenic differentiation of mPDLSCs while markedly suppressing LPS-induced expression. In vivo , AE dose-dependently reduced alveolar bone loss, improved trabecular microarchitecture, increased bone mineral density, and enhanced collagen organization in the periodontitis model. Conclusion AE is a pleiotropic natural compound that reprograms the inflammatory-osteolytic microenvironment of periodontitis and promotes alveolar bone regeneration through multi-target pathway modulation.

Source: Frontiers in Pharmacology

DOI: 10.3389/fphar.2026.1944429