ArticleThe Journal of clinical investigation1997
Paradoxical enhancement of atherosclerosis by probucol treatment in apolipoprotein E-deficient mice.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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
15 citing papers in PubMed, 131 citations in OpenAlex.
- Probucol mitigates high-fat diet-induced cognitive and social impairments by regulating brain redox and insulin resistance.Frontiers in neuroscience · 2024Article
- Probucol treatment is associated with an ABCA1-independent mechanism of cholesterol efflux to lipid poor apolipoproteins from foam cell macrophages.BBA advances · 2021Article
- Associations of ApoAI and ApoB-containing lipoproteins with AngII-induced abdominal aortic aneurysms in mice.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Probucol ameliorates the development of nonalcoholic steatohepatitis in rats fed high-fat diets.Digestive diseases and sciences · 2013Article
- Effects of antioxidant vitamins along with atorvastatin and atorvastatin-niacin combination on diet-induced hypercholesterolemia in rats.International journal of physiology, pathophysiology and pharmacology · 2010Article
- Dose-response impact of various tocotrienols on serum lipid parameters in 5-week-old female chickens.Lipids · 2006Article
- Probucol prevents early coronary heart disease and death in the high-density lipoprotein receptor SR-BI/apolipoprotein E double knockout mouse.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Did the antioxidant trials fail to validate the oxidation hypothesis?Current atherosclerosis reports · 2001Review
- Dissociation of atherogenesis from aortic accumulation of lipid hydro(pero)xides in Watanabe heritable hyperlipidemic rabbits.The Journal of clinical investigation · 1999Article
- Is lipid peroxidation relevant to atherogenesis?The Journal of clinical investigation · 1999Article
- At last, direct evidence that lipoxygenases play a role in atherogenesis.The Journal of clinical investigation · 1999Article
- Antiatherogenic effects of the antioxidant BO-653 in three different animal models.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Effects of antioxidants against atherosclerosis.Molecular and cellular biochemistryReview
- Pharmacological basis of different targets for the treatment of atherosclerosis.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Dietary administration of probucol (0.5%, wt/wt) efficiently reduced total plasma cholesterol levels in apolipoprotein E-deficient mice (apoE-/-) by 40%, with decreases in high density lipoprotein (HDL) and apoAI by 70 and 50%, respectively. Paradoxically, however, aortic atherosclerotic plaques in the probucol-treated apoE-/- mice formed more rapidly than in the untreated apoE-/- mice, and the lesions were two to four times larger and more mature regardless of sex, age, and genetic background (P < 10(-)6). Histologically, lesions in probucol-treated mice contained increased fibrous materials and cells other than foam cells, and were commonly associated with focal inflammation and aneurysmal dilatation. Probucol treatment also accelerated lesion development in apoE+/- mice fed an atherogenic diet, indicating that the adverse effect is not dependent on the complete absence of apoE. Furthermore, mice lacking apoE and apoAI have plasma lipoprotein profiles very similar to the probucol-treated apoE-/- mice, but do not have accelerated plaque development. Thus, the enhanced atherosclerosis in the probucol-treated animals is unlikely to be caused by the reduction of HDL and apoAI levels. Our data indicate that a reduction in plasma cholesterol caused by probucol does not necessarily lead to an antiatherogenic effect.
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Registered trials
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