Taiwanese green propolis suppresses NLRP3 inflammasome activation and induces Nrf2/HO-1 pathway to reduce periodontal pathogen-induced endothelial inflammation.
Journal
Archives of oral biology
Journal Volume
178
Start Page
106364
ISSN
1879-1506
Date Issued
2025-10
Author(s)
Lai, Yi-Jen
Chuang, Yin-Chu
Wang, Yung-Li
Li, Ming-Tse
Lee, Emily Sunny
Lee, Wei-Ju
Lin, Wei-Ning
Wang, Ching-Shuen
Tien Vo, Thi Thuy
Chen, Yue-Wen
Lee, I-Ta
Abstract
Periodontitis is a chronic inflammatory disease associated with systemic conditions, including cardiovascular diseases. Porphyromonas gingivalis (Pg), a key periodontal pathogen, contributes to vascular endothelial dysfunction through its virulence factors. This study aimed to investigate the protective effects of Taiwanese green propolis (TGP) against Pg-derived lipopolysaccharide (Pg-LPS)-induced endothelial inflammation, focusing on its modulation of the NLRP3 inflammasome and Nrf2/HO-1 signaling pathways. Human aortic endothelial cells (HAECs) were stimulated with Pg-LPS in the presence or absence of TGP. The expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) was assessed using real-time PCR and ELISA. ROS production was evaluated using fluorescence-based assays, while NF-κB activation and Nrf2 transcriptional activity were analyzed via luciferase reporter assays. Pharmacological inhibitors were used to confirm the involvement of these pathways. TGP significantly reduced Pg-LPS-induced IL-1β, TNF-α, and IL-6 expression in HAECs. It inhibited NF-κB activation, suppressed ROS generation, and attenuated NLRP3 inflammasome activation. Additionally, TGP upregulated HO-1 expression and enhanced Nrf2 transcriptional activity, as evidenced by ARE-driven luciferase reporter assays. Pharmacological inhibition of Nrf2 and HO-1 reversed TGP's anti-inflammatory effects, confirming that the Nrf2/HO-1 axis is critical for its protective function. These findings demonstrate that TGP exerts anti-inflammatory and cytoprotective effects by suppressing NLRP3 inflammasome activation and enhancing the Nrf2/HO-1 pathway, reducing Pg-LPS-induced endothelial inflammation. This study suggests that TGP could be a promising natural therapeutic agent for mitigating periodontal pathogen-induced systemic inflammation.
Subjects
Inflammation
NLRP3 inflammasome
Oxidative stress
Porphyromonas gingivalis
Taiwanese green propolis
SDGs
Type
journal article