Experimental study of USPIO-enhanced MRI in the detection of atherosclerotic plaque and the intervention of atorvastatin

Ultrasmall superparamagnetic iron oxide (USPIO) can identify atherosclerotic vulnerable plaque and atorvastatin can stabilize vulnerable plaque by inhibiting the inflammatory response. Using balloon injury in rabbit abdominal aortic endothelial cells and p53 gene transfecting the local plaque, we es...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2016-07, Vol.12 (1), p.141-146
Main Authors: SHA, TING, QI, CHUNMEI, FU, WEI, HAO, JI, GONG, LEI, WU, HAO, ZHANG, QINGDUI
Format: Article
Language:English
Subjects:
Abdomen
Animals
Atherosclerosis
Atherosclerotic plaque
Care and treatment
Cell adhesion & migration
cell adhesion molecule-1
Cholesterol
Collagen
Coronary vessels
Diagnosis
Health aspects
Iron oxides
Lipids
Magnetic resonance imaging
Penicillin
Rabbits
Smooth muscle
superparamagnetic iron oxide
Veins & arteries
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Summary:Ultrasmall superparamagnetic iron oxide (USPIO) can identify atherosclerotic vulnerable plaque and atorvastatin can stabilize vulnerable plaque by inhibiting the inflammatory response. Using balloon injury in rabbit abdominal aortic endothelial cells and p53 gene transfecting the local plaque, we established an atherosclerotic vulnerable plaque model. In the treatment group, animals were treated with atorvastatin for 8 weeks. At the end of week 16, the animals in each group underwent medication trigger. USPIO-enhanced MRI was utilized to detect vulnerable plaque formation and the transformation of stable plaque in the treatment group. Pathological and serological studies were conducted in animal sera and tissues. The images from the USPIO-enhanced MRI, and the vulnerable plaque showed low signal, especially on T2*-weighted sequences (T2*WI). Plaque signal strength reached a negative enhancement peak at 96 h. Compared with the other groups, lipids, cell adhesion molecule-1 and vascular cell adhesion molecule-1 levels were significantly lower (P
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2016.3266