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Spermidine Suppresses Development of Experimental Abdominal Aortic Aneurysms
Shuai Liu1, Tingting Huang1, Rui Liu1
1Department of General & Vascular Surgery Xiangya Hospital Central South University Changsha Hunan China.
Journal of the American Heart Association
|April 21, 2020
Summary
Spermidine, a natural polyamine, was found to prevent abdominal aortic aneurysm (AAA) formation in mice by preserving aortic structure and reducing inflammation. This study suggests spermidine may be a promising therapeutic for AAA disease.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Polyamines show protective effects in cardiovascular disease.
- The role of spermidine in abdominal aortic aneurysm (AAA) remains uninvestigated.
- This study explores spermidine's impact on experimental AAA.
Purpose of the Study:
- To investigate the effects of spermidine on experimental AAA.
- To elucidate the potential mechanisms underlying spermidine's influence on AAA.
Main Methods:
- Experimental AAAs were induced in mice using porcine pancreatic elastase.
- Spermidine was administered orally.
- Aortic tissues and blood samples were analyzed using immunostaining, flow cytometry, Western blot, and electron microscopy.
- Human aortic samples were used to assess autophagic function.
Main Results:
- Spermidine treatment prevented AAA formation and preserved medial elastin and smooth muscle cells.
- Spermidine significantly reduced inflammatory cell infiltration (macrophages, T cells, neutrophils) in the aorta.
- Leukocyte infiltration and circulating inflammatory cells were decreased by spermidine.
- Spermidine promoted autophagy-related proteins in experimental AAAs.
- Human aneurysmal aortae showed dysregulated autophagy compared to non-aneurysmal segments.
Conclusions:
- Spermidine supplementation limits experimental AAA formation.
- Spermidine preserves aortic structural integrity and attenuates inflammatory responses.
- Increased autophagy is associated with spermidine treatment in AAA.
- Spermidine shows potential as a therapeutic agent for AAA disease.

