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Apigenin decreases expression of the myofibroblast phenotype

D A Ricupero1, C F Poliks, D C Rishikof

  • 1Pulmonary Center, Boston University School of Medicine and the Boston VA Medical Center, 02118, Boston, MA 02118, USA. ricupero@bu.edu

FEBS Letters
|October 10, 2001
PubMed

Insights

The dietary flavonoid apigenin inhibits myofibroblast proliferation and collagen production by reducing mRNA stability and gene transcription. Apigenin also decreases Akt activity, impacting myofibroblast function.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Myofibroblasts play a key role in tissue repair and fibrosis.
  • Dysregulated myofibroblast function contributes to fibrotic diseases.
  • Dietary compounds are being explored for their therapeutic potential.

Purpose of the Study:

  • To investigate the effects of the dietary flavonoid apigenin on myofibroblast function.
  • To determine the molecular mechanisms by which apigenin influences myofibroblast activity.

Main Methods:

  • Treatment of myofibroblasts with apigenin.
  • Measurement of mRNA levels for alpha1(I) collagen and alpha-smooth muscle actin.
  • Assessment of mRNA stability and gene transcription rates.
  • Western blot analysis to evaluate Akt activity.

Main Results:

  • Apigenin significantly reduced myofibroblast proliferation.
  • Apigenin decreased basal and transforming growth factor-beta-stimulated mRNA levels of alpha1(I) collagen and alpha-smooth muscle actin.
  • Apigenin reduced alpha1(I) collagen mRNA stability and gene transcription via a cycloheximide-sensitive pathway.
  • Apigenin attenuated Akt activity in myofibroblasts.

Conclusions:

  • Apigenin exhibits anti-myofibroblast properties.
  • Apigenin's mechanisms involve reducing collagen and alpha-smooth muscle actin expression at the mRNA level.
  • Apigenin may represent a therapeutic agent for fibrotic conditions.

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