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Abstract <p>Oral squamous cell carcinoma (OSCC) is characterized by a chronic inflammatory microenvironment that drives tumor progression. Lipopolysaccharide (LPS) activates the TLR4/NF-κB signaling axis, triggering the excessive release of pro-inflammatory cytokines—such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)—which promote tumor cell proliferation, invasion, and immune escape. This study aimed to investigate the anti-inflammatory properties of ursolic acid (UA) and its underlying mechanisms in LPS-stimulated OSCC cells. The results demonstrated that UA significantly suppressed the proliferation of the human tongue squamous cell carcinoma cell line CAL-27 and attenuated LPS-induced cellular injury. Mechanistically, UA inhibited the phosphorylation of IκBα, thereby blocking the nuclear translocation of the NF-κB p65 subunit. Consequently, UA reduced the expression and secretion of downstream inflammatory mediators, including TNF-α, IL-6, IL-1β, and COX-2. These findings suggest that UA exerts potent anti-inflammatory effects by modulating the NF-κB pathway, highlighting its potential as a novel therapeutic agent for OSCC.</p>

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Inhibition of the NF-κB Signaling Pathway Mediates the Anti-Inflammatory Effect of Ursolic Acid on LPS-Stimulated Oral Squamous Cell Carcinoma Cells

  • 期刊论文

  • 发表日期：

    2026年7月9日

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  • X. Yao,
  • J. Lei,
  • L. Nie,
  • Y. Li,
  • J. Zhong,
  • D. Wang

摘要

Abstract

Oral squamous cell carcinoma (OSCC) is characterized by a chronic inflammatory microenvironment that drives tumor progression. Lipopolysaccharide (LPS) activates the TLR4/NF-κB signaling axis, triggering the excessive release of pro-inflammatory cytokines—such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)—which promote tumor cell proliferation, invasion, and immune escape. This study aimed to investigate the anti-inflammatory properties of ursolic acid (UA) and its underlying mechanisms in LPS-stimulated OSCC cells. The results demonstrated that UA significantly suppressed the proliferation of the human tongue squamous cell carcinoma cell line CAL-27 and attenuated LPS-induced cellular injury. Mechanistically, UA inhibited the phosphorylation of IκBα, thereby blocking the nuclear translocation of the NF-κB p65 subunit. Consequently, UA reduced the expression and secretion of downstream inflammatory mediators, including TNF-α, IL-6, IL-1β, and COX-2. These findings suggest that UA exerts potent anti-inflammatory effects by modulating the NF-κB pathway, highlighting its potential as a novel therapeutic agent for OSCC.