2. Academic Validation
  3. Benzylurea Protects hPDLFs Against LPS-Induced Mitochondrial Dysfunction Through MTCH2

Benzylurea Protects hPDLFs Against LPS-Induced Mitochondrial Dysfunction Through MTCH2

  • Oral Dis. 2025 Apr;31(4):1255-1267. doi: 10.1111/odi.15172.
Li Liu 1,  Jing Bai 1,  Jiyun Wang 2,  Junheng Fan 1,  Dong Yin 1,  Hong Chang 3,  Xuancheng Hui 4,  Pengfei Yang 5
Affiliations

Affiliations

  • 1 Department of Stomatology, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan, Ningxia, China.
  • 2 Department of Pharmacy, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan, Ningxia, China.
  • 3 School of Stomatology, Ningxia Medical University, Yinchuan, Ningxia, China.
  • 4 Department of Maxillofacial Surgery, Xiangya School of Stomatology, Central South University, Changsha, Hunan, China.
  • 5 Center for Biomedical Engineering, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
PMID: 39491029 DOI: 10.1111/odi.15172
Abstract

Objective: The aim of this study is to explore the mechanism of benzylurea in the inflammatory injury of human periodontal ligament fibroblasts (hPDLFs).

Methods: An inflammation model of hPDLFs was established using LPS. Nuclear transport of nuclear transcription factor-κB (NF-κB), secretion of cytokines, and the morphology and distribution of F-actin were determined. Mitochondrial function was assessed by measuring mitochondrial membrane potential (MMP), mitochondrial permeability transition pore (mPTP), and Reactive Oxygen Species (ROS) levels. The expression of mitochondrial carrier homolog 2 (MTCH2) and Cytochrome b5 type B (CYB5B) was detected.

Results: Benzylurea alleviated the effects of lipopolysaccharide (LPS) on the proliferation and Apoptosis of hPDLFs. It reduced the release of inflammatory cytokines and inhibited NF-κB nuclear translocation. Benzylurea improved mitochondrial function by regulating MMP and preventing excessive mPTP opening. Furthermore, LPS elevated the expression of MTCH2 and reduced the expression of CYB5B in hPDLFs. However, these effects can be inhibited by benzylurea. The altered expression of MTCH2 directly affected CYB5B expression, the release of inflammatory cytokines, and the activation of nuclear translocation of NF-κB.

Conclusion: CYB5B may act as an effector of MTCH2, with benzylurea enhancing mitochondrial function and protecting hPDLFs from LPS-induced injury through MTCH2.

Keywords

lipopolysaccharides; mitochondria; periodontal ligament; periodontitis.

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