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Paeoniflorin inhibits VSMCs proliferation and migration by arresting cell cycle and activating HO-1 through MAPKs and

Weifeng Li1, Wenbing Zhi1, Fang Liu1

  • 1School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, PR China.

International Immunopharmacology
|November 10, 2017
PubMed

Insights

Paeoniflorin (PF) inhibits vascular smooth muscle cell proliferation, migration, and inflammation induced by oxidized LDL (ox-LDL). This natural compound also prevents foam cell formation, offering potential therapeutic benefits for atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Cell Biology

Background:

  • Atherosclerosis involves vascular smooth muscle cell (VSMC) proliferation, migration, and inflammation.
  • Oxidized low-density lipoprotein (ox-LDL) is a key factor in atherosclerosis pathogenesis.
  • Paeoniflorin (PF), derived from Rhizoma Atractylodes macrocephala, has diverse medicinal applications.

Purpose of the Study:

  • To investigate the effects of PF on VSMC behavior under ox-LDL stimulation.
  • To elucidate the underlying molecular mechanisms of PF's action.
  • To assess PF's impact on ox-LDL-induced foam cell formation in macrophages.

Main Methods:

  • VSMC proliferation, migration, and inflammatory cytokine/chemokine expression assays.
  • Western blotting to analyze p38, ERK1/2, NF-κB phosphorylation, HO-1, and PCNA.
  • Cell cycle analysis.
  • Macrophage foam cell formation assay.

Main Results:

  • PF dose-dependently inhibited ox-LDL-induced VSMC proliferation and migration.
  • PF reduced inflammatory cytokine and chemokine levels.
  • PF suppressed p38, ERK1/2, and NF-κB phosphorylation, arresting cell cycle in S phase.
  • PF regulated HO-1 and PCNA expression and blocked macrophage foam cell formation.

Conclusions:

  • PF exhibits anti-atherosclerotic properties by inhibiting VSMC dysfunction and inflammation.
  • PF acts through HO-1 activation, cell cycle arrest, and suppression of MAPK and NF-κB pathways.
  • PF demonstrates potential as a therapeutic agent for atherosclerosis treatment.
Keywords:
AtherosclerosisInflammationMigrationPaeoniflorinProliferationVascular smooth muscle cell

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