Korean Circ J.  2000 Apr;30(4):517-527. 10.4070/kcj.2000.30.4.517.

The effects of antiproliferative drugs at stenotic area associated with primary atherosclerotic lesions in apoE knockout mouse - Change of vascular remodeling

Abstract

Apolipoprotein (apo) E deficient mouse can produce reproducible fixed stenotic primary atherosclerotic lesion, which reveals failure to remodel of vascular lumen, in the ascending aorta, external carotid, common carotid, iliac, femoral and popliteal arteries. To evaluate the effect of drugs in regarding to both prevention of primary atherosclerotic lesion and vascular remodeling, a systematic analysis of distribution of atherosclerotic lesions was undertaken in chow-fed, 9-momth-old apo E deficient mice, which was administrated drugs including asprin, methotrexate, probucol, sulodexide, diltiazem, cilazapril, trimetazidine, molsidomine, pentoxiphylline and Ginexin (R) for 7 month from 3 month-old. On gross and microscopic examination, formation of primary atheroscleotic lesions could be delated and/or prevented patially by effets of these drugs. On morphometric examination, failure to remodel forming vascular stenosis could not be seen, though relatively mild atherosclerotic lesion occured at vascular tree. These data suggest that the stenotic process in advanced atherosclerotic vessels can be delayed and/or prevented by several drugs including methotrexate, probucol, sulodexide, diltiazem, cilazapril, trimetazidine, molsidomine, pentoxiphylline and Ginexin (R) in vivo state.

Keyword

apolipoprotein E deficient mouse; Atherosclerosis; Vascular remodel; Primary prevention

MeSH Terms

Animals
Aorta
Apolipoproteins
Apolipoproteins E*
Atherosclerosis
Cilazapril
Constriction, Pathologic
Diltiazem
Humans
Infant
Methotrexate
Mice
Mice, Knockout*
Molsidomine
Popliteal Artery
Primary Prevention
Probucol
Trimetazidine
Apolipoproteins
Apolipoproteins E
Cilazapril
Diltiazem
Methotrexate
Molsidomine
Probucol
Trimetazidine
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