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Updated: Sep 17, 2025
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Hylotelephium mingjinianum Extract Attenuates Oxidative Stress and Inflammation in Experimental Periodontitis
Lin Yuan1, Chenfei Kong2, Naixu Shi1
1Department of Stomatology, China-Japan Union Hospital of Jilin University, Changchun, People's Republic of China.
Background:
Hylotelephium mingjinianum is a traditional Chinese herbal medicine with anti-inflammatory, analgesic and antibacterial effects. However, its role in the treatment of Periodontal disease has not been elaborated in detail.
Purpose:
This study aimed to elucidate the dual-target anti-inflammatory and antioxidant mechanisms of Hylotelephium mingjinianum extract (HME) in periodontitis treatment, focusing on its modulation of the Nrf2/NF-κB crosstalk.
Methods:
The periodontitis animal model of SD rats was established by ligation combined with Porphyromonas gingivalis (Pg) stimulation. The rats were locally administered HME (0.25%, 0.5%, and 1%, 0.5 mL/twice/day) for 14 days. Inflammatory responses of alveolar bone, expression of osteogenic related biomarkers, and activation of Nrf2/NF-κB signaling pathway were detected. In addition, LPS induced human periodontal ligament cells (HPDLs) to measure the effect of HME on cell viability, inflammatory response, Nrf2/NF- κB pathway and oxidative stress.
Results:
HME administration demonstrated significant efficacy in a ligature-induced periodontitis rat model: serum pro-inflammatory cytokines (IL-1β, IL-2, IL-6, IL-18, GM-CSF, and ICAM1) decreased by 24.9-50.6% at high HME concentrations, while Th2-related factors IL-4/IL-13 returned to baseline levels. Histopathological analysis revealed that HME maintained gingival epithelial integrity and suppressed osteoclast activity in a dose-dependent manner by downregulating RANKL. Mechanistic studies indicated that HME attenuated NF-κB activation by reducing nuclear p65 protein (44.1%) and enhanced the Nrf2-mediated antioxidant response, normalizing oxidative stress markers (MDA decreased by 55.3%; SOD restored to 142.3 U/mg). In vitro experiments confirmed HME's cytocompatibility at concentrations below 200µg/mL and its resistance to LPS stimulation, reducing ROS overaccumulation by 16.46% through modulation of the Nrf2/NF-κB axis.
Conclusion:
HME inhibits the progression of periodontitis in rats by downregulating the expression of inflammatory factors, alleviating oxidative stress, and repairing the Nrf2/NF-κB signaling pathway.
