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Cinnamic aldehyde inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in Zucker Diabetic

Nicholas E Buglak1, Wulin Jiang2, Edward S M Bahnson3

  • 1Department of Surgery, Division of Vascular Surgery, University of North Carolina at Chapel Hill, NC 27599, USA; Center for Nanotechnology in Drug Delivery, University of North Carolina at Chapel Hill, NC 27599, USA; Curriculum in Toxicology & Environmental Medicine, University of North Carolina at Chapel Hill, NC 27599, USA.

Redox Biology
|September 2, 2018
PubMed

Insights

Cinnamic aldehyde (CA) effectively inhibits neointimal hyperplasia in diabetic rats by activating Nrf2, reducing vascular smooth muscle cell proliferation, and decreasing vessel occlusion. This offers a promising therapeutic strategy for preventing restenosis after revascularization procedures.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Disease Research
  • Pharmacology

Background:

  • Atherosclerosis is a leading cause of death, with restenosis after revascularization procedures being a significant complication.
  • Diabetes mellitus exacerbates atherosclerosis and restenosis by promoting vascular smooth muscle cell (VSMC) proliferation and migration.
  • Reactive oxygen species (ROS) drive VSMC proliferation; thus, redox intervention is a potential strategy to inhibit restenosis.

Purpose of the Study:

  • To investigate the efficacy of cinnamic aldehyde (CA), an Nrf2 activator, in inhibiting neointimal hyperplasia in a rat model of diabetic restenosis.
  • To determine if CA activates the Nrf2 pathway and modulates redox homeostasis in vascular cells and tissues.

Main Methods:

  • Primary Zucker Diabetic Fatty (ZDF) VSMC were used to assess CA's effect on cell growth and migration in vitro.
  • A carotid artery balloon injury model in ZDF rats was employed to evaluate CA's in vivo efficacy.
  • Nrf2 activation, antioxidant defenses, inflammatory cell infiltration, and neointimal hyperplasia were quantified.

Main Results:

  • CA inhibited ZDF VSMC proliferation (EC50 = 118 ± 7 μM) and migration in vitro.
  • In vivo, CA reduced the proliferative index in injured arteries and significantly decreased neutrophil and macrophage infiltration.
  • CA treatment resulted in a 53% reduction in the intima:media ratio and a 61% decrease in vessel occlusion.

Conclusions:

  • Cinnamic aldehyde activates the Nrf2 pathway and enhances antioxidant defenses.
  • CA effectively inhibits neointimal hyperplasia and vessel occlusion in a diabetic rat model of restenosis.
  • CA demonstrates therapeutic potential for preventing diabetic restenosis by targeting VSMC proliferation and inflammation.
Keywords:
Cinnamic aldehydeDiabetesNeointimal hyperplasiaNrf2RestenosisVascular smooth muscle cells

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