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Luteolin Induces Nrf2 Activity in C2C12 Cells: Implications for Muscle Health.

Nicole Böttcher1, Frank Suhr1,2, Thomas Pufe1

  • 1Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, 52074 Aachen, Germany.

International Journal of Molecular Sciences
|May 14, 2025
PubMed
Summary

Luteolin activates the Nrf2 pathway in muscle cells, unlike creatine, L-BAIBA, or silibinin. This suggests luteolin may help combat muscle wasting conditions like sarcopenia and cachexia.

Keywords:
C2C12 myoblastsNrf2Nrf2 activatorsSkMluteolinskeletal muscle

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Chronic oxidative stress causes cellular damage, requiring redox balance mechanisms.
  • The transcription factor Nrf2 regulates antioxidant and cytoprotective genes.
  • Nrf2-Keap1 pathway activation may slow aging-related muscle degeneration (sarcopenia, cachexia).

Purpose of the Study:

  • Investigate creatine, L-BAIBA, luteolin, and silibinin's efficacy in inducing Nrf2.
  • Assess Nrf2 activation and target gene expression in C2C12 myoblasts.
  • Determine potential of these compounds against muscle wasting.

Main Methods:

  • Utilized murine myoblast cell line C2C12.
  • Administered creatine, L-BAIBA, luteolin, and silibinin.
  • Measured Nrf2 activity and target gene expression in proliferating and differentiated cells.

Main Results:

  • Luteolin significantly enhanced Nrf2 activity in both C2C12 cell states.
  • Luteolin increased Nrf2 target gene expression in proliferating cells.
  • Creatine, L-BAIBA, and silibinin showed minimal to no effect on Nrf2 activity.

Conclusions:

  • C2C12 cells exhibit distinct responses to Nrf2 activators.
  • Cellular context is crucial for the biological effects of Nrf2 modulators.
  • Luteolin shows promise as a therapeutic agent for muscle wasting.