Key result
S18886 prevents a ~4-fold increase in aortic lesions in diabetic mice without altering glucose or cholesterol.
Why the study?
Does S18886 prevent enhanced atherogenesis in diabetic apoE-/- mice?
Population
Apolipoprotein E-deficient mice with streptozotocin-induced diabetes mellitus; human aortic endothelial…
Comparison
S18886 (5 mg/kg/day) for 6 weeks vs Untreated diabetic apoE-/- mice
Design
Preclinical
Follow-up
6 weeks
Authors
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Preclinical findings do not support clinical use of S18886; leaves open whether thromboxane receptor antagonism reduces diabetic atherogenesis in humans.
Does S18886 prevent enhanced atherogenesis in diabetic apoE-/- mice?
The thromboxane A2 receptor antagonist S18886 prevents accelerated atherogenesis and endothelial dysfunction caused by diabetes in a preclinical model.
Zuccollo et al. (2005) studied Diabetes mellitus and atherosclerosis. S18886 vs. No treatment was evaluated on Aortic lesion area. S18886 largely prevented the diabetes-related >4-fold increase in aortic lesion area in apoE(-/-) mice without affecting hyperglycemia or hypercholesterolemia.
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