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Updated: Feb 8, 2026

A Calcium Phosphate-Induced Mouse Abdominal Aortic Aneurysm Model
Published on: November 18, 2022
Embelin inhibits abdominal aortic aneurysm through decreasing IL‑6‑induced STAT3 and NF‑κB inactivation
Qiang Liu1, Qingshan Wang2, Haibin Li1
1Department of Vascular Surgery, The First Hospital of Qiqiha'er City, Qiqiha'er, Heilongjiang 161005, P.R. China.
Abstract:
The aim of the present study was to investigate the effect of embelin on abdominal aortic aneurysm (AAA). AAA model mice were induced by chronic infusion of 1,000 ng/kg/min Angiotensin II. AAA model mice were treated with 25, 50 or 100 mg/kg embelin for 28 days. Embelin inhibited tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6, IL‑18 and malondialdehyde (MDA) level activities, increased superoxide dismutase, glutathione (GSH) and GSH peroxidase level activities and inhibited MDA level activities in AAA mice Embelin suppressed the secretion of matrix metalloproteinase‑9 protein expression, monocyte chemoattractant protein‑2 activity and epithelial neutrophil‑activating peptide expression levels in AAA mice. Embelin suppressed phosphorylated‑signal transducer and activator of transcription (STAT) 3, phosphorylated‑p38 mitogen‑activated protein kinase and nuclear factor (NF)‑κB protein expression in AAA mice. These findings indicate that embelin inhibits AAA through decreasing IL‑6‑induced STAT3, and NF‑κB inactivation.
Insights
Embelin effectively treats abdominal aortic aneurysm (AAA) by reducing inflammation and oxidative stress. This natural compound targets key inflammatory pathways, offering a potential therapeutic strategy for AAA.
Area of Science:
- Biomedical Science
- Pharmacology
- Cardiovascular Research
Background:
- Abdominal aortic aneurysm (AAA) is a life-threatening condition characterized by aortic wall degradation.
- Current treatments for AAA are limited, necessitating the exploration of novel therapeutic agents.
Purpose of the Study:
- To investigate the therapeutic potential of embelin in a mouse model of abdominal aortic aneurysm (AAA).
Main Methods:
- AAA was induced in mice via chronic Angiotensin II infusion.
- Mice were treated with varying doses of embelin (25, 50, 100 mg/kg) for 28 days.
- Key inflammatory markers, oxidative stress indicators, and signaling pathways were assessed.
Main Results:
- Embelin significantly reduced levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-18) and malondialdehyde (MDA).
- Embelin increased antioxidant enzyme activity (superoxide dismutase, GSH, GSH peroxidase).
- Embelin suppressed matrix metalloproteinase-9, monocyte chemoattractant protein-2, and epithelial neutrophil-activating peptide expression.
- Embelin inhibited key signaling pathways including phosphorylated-STAT3, phosphorylated-p38 MAPK, and NF-κB.
Conclusions:
- Embelin demonstrates significant efficacy in inhibiting AAA progression in a mouse model.
- The therapeutic effects of embelin are mediated by the suppression of inflammatory responses and oxidative stress.
- Embelin's mechanism involves the inactivation of IL-6-induced STAT3 and NF-κB signaling pathways.
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