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<p>Oral lichen planus (OLP) is a chronic inflammatory oral mucosal disease with immune-mediated pathogenesis and potential for malignant transformation. Elevated inflammatory cytokines and oxidative stress contribute to its progression. This study explored the therapeutic potential of glucagon-like peptide-1 (GLP-1) in modulating inflammation and oxidative stress in OLP. To establish an in vitro OLP model, human oral keratinocytes (HOK) were treated with lipopolysaccharide (LPS) at varying concentrations, and 5&#xa0;µg/ml was selected as the optimal concentration based on CCK-8 assay results. The inflammatory response was assessed using qRT-PCR and ELISA to measure IL-6, TNF-α, and IL-1β expression. Oxidative stress levels were determined using DCF-DA fluorescence staining for ROS detection and SOD activity assays. The involvement of the JAK/STAT3 pathway was evaluated using western blot analysis of JAK, p-JAK, STAT3, and p-STAT3 protein expression. The OLP model was successfully established in HOK cells using LPS, with significant morphological changes and reduced cell viability observed at 10&#xa0;µg/ml and higher concentrations. LPS stimulation induced inflammation and oxidative stress, marked by elevated IL-6, TNF-α, IL-1β mRNA and protein levels, increased ROS production, and reduced SOD activity. GLP-1 treatment (10 nM to 100 nM) significantly reduced inflammation and oxidative stress in a dose-dependent manner. GLP-1 inhibited the expression of pro-inflammatory cytokines and decreased ROS levels while enhancing SOD activity. Further analysis revealed that GLP-1’s effects were mediated through the JAK/STAT3 pathway, as demonstrated by the suppression of JAK and STAT3 phosphorylation, which was comparable to the effects of the JAK/STAT3 inhibitor Stattic. This study elucidated that GLP-1 mitigated inflammation and oxidative stress in an in vitro model of OLP via JAK/STAT3 signaling pathway, demonstrating its potential as a therapeutic agent in OLP.</p> Graphcial Abstract <p></p> <p>Glucagon-like peptide-1 (GLP-1) treatment inhibited activation of JAK/STAT3 signaling pathway, which in turn prevent oxidative stress and inflammation, thereby alleviating oral lichen planus (OLP).</p>

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GLP-1 Mitigated Inflammation and Oxidative Stress in Oral Lichen Planus Via JAK-STAT3 Pathway

  • 期刊论文

  • 发表日期：

    2026年2月7日

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  • Yaxuan Liu,
  • Ning Liu,
  • Wenjing Wang,
  • Rongxia Zhang,
  • Xiaoying Liu,
  • Liwei Wu,
  • Chencong Li

摘要

Oral lichen planus (OLP) is a chronic inflammatory oral mucosal disease with immune-mediated pathogenesis and potential for malignant transformation. Elevated inflammatory cytokines and oxidative stress contribute to its progression. This study explored the therapeutic potential of glucagon-like peptide-1 (GLP-1) in modulating inflammation and oxidative stress in OLP. To establish an in vitro OLP model, human oral keratinocytes (HOK) were treated with lipopolysaccharide (LPS) at varying concentrations, and 5 µg/ml was selected as the optimal concentration based on CCK-8 assay results. The inflammatory response was assessed using qRT-PCR and ELISA to measure IL-6, TNF-α, and IL-1β expression. Oxidative stress levels were determined using DCF-DA fluorescence staining for ROS detection and SOD activity assays. The involvement of the JAK/STAT3 pathway was evaluated using western blot analysis of JAK, p-JAK, STAT3, and p-STAT3 protein expression. The OLP model was successfully established in HOK cells using LPS, with significant morphological changes and reduced cell viability observed at 10 µg/ml and higher concentrations. LPS stimulation induced inflammation and oxidative stress, marked by elevated IL-6, TNF-α, IL-1β mRNA and protein levels, increased ROS production, and reduced SOD activity. GLP-1 treatment (10 nM to 100 nM) significantly reduced inflammation and oxidative stress in a dose-dependent manner. GLP-1 inhibited the expression of pro-inflammatory cytokines and decreased ROS levels while enhancing SOD activity. Further analysis revealed that GLP-1’s effects were mediated through the JAK/STAT3 pathway, as demonstrated by the suppression of JAK and STAT3 phosphorylation, which was comparable to the effects of the JAK/STAT3 inhibitor Stattic. This study elucidated that GLP-1 mitigated inflammation and oxidative stress in an in vitro model of OLP via JAK/STAT3 signaling pathway, demonstrating its potential as a therapeutic agent in OLP.

Graphcial Abstract

Glucagon-like peptide-1 (GLP-1) treatment inhibited activation of JAK/STAT3 signaling pathway, which in turn prevent oxidative stress and inflammation, thereby alleviating oral lichen planus (OLP).