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Peer-reviewedCC BYAntioxidants (Basel, Switzerland)

Bergapten Alleviates Periodontitis by Suppressing NLRP3 Inflammasome Activation via Mitophagy-Induced Disruption of NEK7-NLRP3 Interaction.

  • Xiangbin Jia1,2
  • Yuzhao Wang3,4
  • Jiao Cao5
  • Lifei Pan1,2
  • Xiaoxuan Cui1,2
  • Hanxue Shan1,2
  • Yiqing Wang1,2
  • Xiao Cao1,2
  • Qin Zhou1,2,6
6 affiliations
  1. 1Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, China.
  2. 2Clinical Research Center of Shaanxi Province for Dental and Maxillofacial Diseases, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, China.
  3. 3Department of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.
  4. 4Key Laboratory for Tumor Precision Medicine of Shaanxi Province, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.
  5. 5Engineering Research Center of Tibetan Medicine Detection Technology, Ministry of Education, School of Medicine, Xizang Minzu University, Xianyang 712082, China.
  6. 6Department of Implant Dentistry, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, China.
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Abstract

Periodontitis is a prevalent chronic inflammatory disease characterized by gingival inflammation and progressive alveolar bone loss. The NLRP3 inflammasome functions as a molecular mediator that drives its pathogenesis. Bergapten (BeG), a natural furanocoumarin, exhibits anti-inflammatory properties and bone-protective effects. This study demonstrates that BeG alleviates experimental periodontitis in mice by inhibiting the NLRP3 inflammasome. Mechanistically, BeG does not affect NLRP3 priming, dispersed trans-Golgi network (dTGN) localization, or oligomerization; instead, it induces mitophagy by inhibiting the AKT-mTOR axis and consequently suppresses the mtROS-dependent NEK7-NLRP3 interaction. Notably, BeG also suppressed cytosolic release of oxidized mitochondrial DNA (ox-mtDNA), a known endogenous ligand for NLRP3. This effect was attributed to BeG-mediated inhibition of NLRP3 activation, likely via blockade of GSDMD-NT mitochondrial localization. These findings deepen our understanding of the anti-inflammatory mechanisms of BeG and position it as a promising candidate for periodontitis treatment.

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Cite

BibTeXRIS
BibTeX
@article{jia2026bergapten,
  title = {{Bergapten Alleviates Periodontitis by Suppressing NLRP3 Inflammasome Activation via Mitophagy-Induced Disruption of NEK7-NLRP3 Interaction.}},
  author = {Xiangbin Jia and Yuzhao Wang and Jiao Cao and Lifei Pan and Xiaoxuan Cui and Hanxue Shan and Yiqing Wang and Xiao Cao and Qin Zhou},
  journal = {Antioxidants (Basel, Switzerland)},
  year = {2026},
  month = oct,
  doi = {10.3390/antiox15101304},
  url = {https://europepmc.org/article/MED/42939878},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Bergapten Alleviates Periodontitis by Suppressing NLRP3 Inflammasome Activation via Mitophagy-Induced Disruption of NEK7-NLRP3 Interaction.
AU  - Xiangbin Jia
AU  - Yuzhao Wang
AU  - Jiao Cao
AU  - Lifei Pan
AU  - Xiaoxuan Cui
AU  - Hanxue Shan
AU  - Yiqing Wang
AU  - Xiao Cao
AU  - Qin Zhou
PY  - 2026
DA  - 2026/10/09
JO  - Antioxidants (Basel, Switzerland)
DO  - 10.3390/antiox15101304
UR  - https://europepmc.org/article/MED/42939878
AB  - Periodontitis is a prevalent chronic inflammatory disease characterized by gingival inflammation and progressive alveolar bone loss. The NLRP3 inflammasome functions as a molecular mediator that drives its pathogenesis. Bergapten (BeG), a natural furanocoumarin, exhibits anti-inflammatory properties and bone-protective effects. This study demonstrates that BeG alleviates experimental periodontitis in mice by inhibiting the NLRP3 inflammasome. Mechanistically, BeG does not affect NLRP3 priming, dispersed trans-Golgi network (dTGN) localization, or oligomerization; instead, it induces mitophagy by inhibiting the AKT-mTOR axis and consequently suppresses the mtROS-dependent NEK7-NLRP3 interaction. Notably, BeG also suppressed cytosolic release of oxidized mitochondrial DNA (ox-mtDNA), a known endogenous ligand for NLRP3. This effect was attributed to BeG-mediated inhibition of NLRP3 activation, likely via blockade of GSDMD-NT mitochondrial localization. These findings deepen our understanding of the anti-inflammatory mechanisms of BeG and position it as a promising candidate for periodontitis treatment.
SN  - 2076-3921
ER  -