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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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Detalles Bibliográficos
Autores principales: SHA, TING, QI, CHUNMEI, FU, WEI, HAO, JI, GONG, LEI, WU, HAO, ZHANG, QINGDUI
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4907054/
https://www.ncbi.nlm.nih.gov/pubmed/27347029
http://dx.doi.org/10.3892/etm.2016.3266
Descripción
Sumario: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<0.05) in the treatment group. In conclusion, USPIO-enhanced MRI can identify vulnerable plaque formation by deposition in macrophages, while atorvastatin is able to inhibit the progression of atherosclerosis and promote plaque transformation to the stable form.