ArticlePloS one2012
Cilostazol inhibits accumulation of triglyceride in aorta and platelet aggregation in cholesterol-fed rabbits.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- The Role of Cilostazol, a Phosphodiesterase-3 Inhibitor, in the Development of Atherosclerosis and Vascular Biology: A Review with Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Hypertriglyceridemia and Atherosclerotic Carotid Artery Stenosis.International journal of molecular sciences · 2022Review
- Cilostazol: a Review of Basic Mechanisms and Clinical Uses.Cardiovascular drugs and therapy · 2022Review
- Cilostazol for Secondary Prevention of Stroke: Should the Guidelines Perhaps Be Extended?Vascular specialist international · 2017Review
- Anti-aggregatory effect of boswellic acid in high-fat fed rats: involvement of redox and inflammatory cascades.Archives of medical science : AMS · 2016Article
- Evaluation and Treatment of the Acute Cerebral Infarction with Convexal Subarachnoid Hemorrhage.Journal of cerebrovascular and endovascular neurosurgery · 2016Article
- Probucol inhibits the initiation of atherosclerosis in cholesterol-fed rabbits.Lipids in health and disease · 2013Article
- Allium sativum Compared to Cilostazol as an Inhibitor of Myointimal Hyperplasia.Brazilian journal of cardiovascular surgeryArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cilostazol is clinically used for the treatment of ischemic symptoms in patients with chronic peripheral arterial obstruction and for the secondary prevention of brain infarction. Recently, it has been reported that cilostazol has preventive effects on atherogenesis and decreased serum triglyceride in rodent models. There are, however, few reports on the evaluation of cilostazol using atherosclerotic rabbits, which have similar lipid metabolism to humans, and are used for investigating the lipid content in aorta and platelet aggregation under conditions of hyperlipidemia. Therefore, we evaluated the effect of cilostazol on the atherosclerosis and platelet aggregation in rabbits fed a normal diet or a cholesterol-containing diet supplemented with or without cilostazol. We evaluated the effects of cilostazol on the atherogenesis by measuring serum and aortic lipid content, and the lesion area after a 10-week treatment and the effect on platelet aggregation after 1- and 10-week treatment. From the lipid analyses, cilostazol significantly reduced the total cholesterol, triglyceride and phospholipids in serum, and moreover, the triglyceride content in the atherosclerotic aorta. Cilostazol significantly reduced the intimal atherosclerotic area. Platelet aggregation was enhanced in cholesterol-fed rabbits. Cilostazol significantly inhibited the platelet aggregation in rabbits fed both a normal diet and a high cholesterol diet. Cilostazol showed anti-atherosclerotic and anti-platelet effects in cholesterol-fed rabbits possibly due to the improvement of lipid metabolism and the attenuation of platelet activation. The results suggest that cilostazol is useful for prevention and treatment of atherothrombotic diseases with the lipid abnormalities.
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