Astragaloside IV Attenuated 3,4-Benzopyrene-Induced Abdominal Aortic Aneurysm by Ameliorating Macrophage-Mediated

Jiaoni Wang1, Yingying Zhou2, Shaoze Wu1

  • 1Department of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.

Insights

Astragaloside IV (AS-IV) shows protective effects against abdominal aortic aneurysm (AAA) by reducing inflammation and oxidative stress. This natural compound may serve as a potential intervention for AAA development.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Cardiovascular Research

Background:

  • Abdominal aortic aneurysm (AAA) is a serious condition driven by inflammation and oxidative stress.
  • Macrophage infiltration plays a key role in AAA pathogenesis.
  • Astragaloside IV (AS-IV) is known for its antioxidant and anti-inflammatory properties.

Purpose of the Study:

  • To investigate the protective effects of AS-IV against AAA formation induced by 3,4-benzopyrene (Bap) and angiotensin II (Ang II).
  • To explore the underlying mechanisms of AS-IV's action in AAA.
  • To evaluate AS-IV as a potential therapeutic agent for AAA.

Main Methods:

  • AAA was induced in a model using Bap and Ang II.
  • The effects of AS-IV on AAA formation, macrophage infiltration, and matrix metalloproteinase expression were assessed.
  • Activation of NF-κB, oxidative stress markers, and the PI3-K/AKT pathway were analyzed.
  • In vitro studies utilized RAW264.7 macrophage cells.

Main Results:

  • AS-IV significantly reduced AAA formation and decreased macrophage infiltration and matrix metalloproteinase expression.
  • AS-IV inhibited Bap/Ang II-induced NF-κB activation and oxidative stress.
  • In vitro, AS-IV suppressed macrophage activation by inhibiting oxidative stress and NF-κB via the PI3-K/AKT pathway.

Conclusions:

  • AS-IV demonstrates protective effects against AAA, primarily through suppressing inflammation in the aortic wall.
  • AS-IV effectively abrogates NF-κB activation and oxidative stress induced by Bap/Ang II.
  • AS-IV's mechanism involves inhibiting macrophage activation via the PI3-K/AKT pathway, suggesting its potential as a preventive agent for smoking-related AAA.

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