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NRF2 Activation Suppressed Methylglyoxal-Lysine Dimer-Induced Oxidative Stress and Inflammatory Paracrine Interaction

Hee-Weon Lee1,2, Min Ji Gu1, Donghwan Kim1

  • 1Korea Food Research Institute, Jeonbuk 55365, Korea.

Preventive Nutrition and Food Science
|November 3, 2025
PubMed

Insights

Methylglyoxal-lysine dimer (MOLD) triggers inflammation and adipogenesis by increasing advanced glycation end products (AGEs). NRF2 activation mitigates these MOLD-induced effects, suggesting its role in metabolic disorders.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Disorders

Background:

  • Macrophage infiltration is linked to obesity-related inflammation.
  • Advanced glycation end products (AGEs) play a role in metabolic dysfunction.

Purpose of the Study:

  • To investigate methylglyoxal-lysine dimer (MOLD)-induced inflammation and metabolic disorders.
  • To explore the interaction between macrophages and adipocytes in response to MOLD.
  • To assess the role of NF-E2 p45-related factor 2 (NRF2) in MOLD-induced responses.

Main Methods:

  • Utilized an in vitro conditioned co-culture medium model.
  • Exposed RAW 264.7 cells (macrophages) and 3T3-L1 cells (adipocytes) to MOLD.
  • Measured levels of AGEs, inflammatory markers, and adipogenesis-related genes.
  • Investigated the effect of NRF2 activation.

Main Results:

  • MOLD increased AGEs, nitric oxide, prostaglandin E2, and inflammatory cytokines (TNF-α, IL-6) in macrophages.
  • Macrophage-conditioned medium promoted adipogenesis and lipid accumulation in adipocytes.
  • NRF2 activation inhibited MOLD-induced inflammation and adipogenesis gene expression.

Conclusions:

  • MOLD stimulates inflammatory responses and adipogenesis.
  • NRF2 activation acts as a suppressor of MOLD-induced inflammation and adipogenesis.
  • NRF2 may be a critical regulator in MOLD-associated metabolic disorders.
Keywords:
advanced glycation end productsinflammationmacrophagesobesityreceptors

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