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  11. Reactive Oxygen Species/c-jun N-terminal Kinase/nuclear Factor Kappa-b Signaling Molecules Are Involved In Pe-riodontitis-induced Liver Injury By Regulating Apoptosis

Reactive oxygen species/c-Jun N-terminal kinase/nuclear factor kappa-B signaling molecules are involved in pe-riodontitis-induced liver injury by regulating apoptosis

Niuben Cao1, Xiaomeng Liu1, Yu Deng1

  • 1Dept. of Periodontics, Hospital of Stomatology, Jilin University, Changchun 130021, China.

Hua Xi Kou Qiang Yi Xue Za Zhi = Huaxi Kouqiang Yixue Zazhi = West China Journal of Stomatology
|April 10, 2024

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Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
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View abstract on PubMed

Summary
This summary is machine-generated.

Periodontitis triggers liver injury by increasing reactive oxygen species (ROS) and activating the JNK/NF-κB pathway, leading to apoptosis. This study elucidates this mechanism, highlighting potential therapeutic targets for periodontitis-related liver damage.

Area of Science:

  • Investigates the molecular mechanisms linking periodontitis to liver injury.
  • Focuses on the role of oxidative stress and specific signaling pathways in disease pathogenesis.

Background:

  • Periodontitis and nonalcoholic fatty liver disease (NAFLD) share common links to reactive oxygen species (ROS) accumulation.
  • ROS overactivation of c-Jun N-terminal kinase (JNK)/nuclear factor kappa-B (NF-κB) signaling can disrupt the body's internal environment.

Purpose of the Study:

  • To explore the mechanism by which ROS/JNK/NF-κB signaling molecules mediate periodontitis-induced liver injury.
  • To understand the role of apoptosis in this pathological process.

Main Methods:

  • Established a periodontitis model in Wistar rats using wire ligation.
  • Assessed periodontal indexes, alveolar bone resorption (Micro-CT), and histopathological changes in periodontal and liver tissues.
Keywords:
apoptosisc-Jun N-terminal kinasesliver injurynuclear factor kappa-B

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  • Quantified ROS levels, liver function markers, oxidative stress biomarkers, and gene/protein expression of key signaling molecules (IL-6, TNF-α, NF-κB, Bax, Bcl-2, JNK, Caspase-3) using biochemical assays, qRT-PCR, Western blot, and TUNEL staining.

    • Main Results:

    • Periodontitis group exhibited significant alveolar bone resorption and liver tissue damage with increased ROS, AST, ALT, and MDA levels.
    • Elevated expression of inflammatory markers (IL-6, TNF-α), pro-apoptotic factors (Bax, Caspase-3), and activated JNK/NF-κB signaling was observed in the liver.
    • Increased apoptosis and decreased antioxidant capacity (SOD, GSH) were noted in the periodontitis group, alongside reduced Bcl-2 expression.

    Conclusions:

    • The ROS/JNK/NF-κB signaling pathway plays a critical role in periodontitis-induced liver injury.
    • This pathway mediates liver damage by regulating apoptosis, suggesting it as a key therapeutic target.
    oxidative stress
    periodontitis