Absence of an atheroprotective effect of the garlic powder printanor in APOE*3-Leiden transgenic mice

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Numerous animal studies have reported that garlic can protect against atherosclerosis. However, a comparable number of studies do not support this observation. This contradiction may result from differences in study design, use of different animal models, and use of different garlic formulations and preparations. Here, we investigated the effect of the chemically well-characterized and production-controlled garlic powder printanor on atherosclerosis in the APOE*3-Leiden transgenic mouse, a mouse model well suited for evaluating anti-atherosclerotic properties of drugs and food components under human-like conditions. APOE*3-Leiden mice were fed a Western diet supplemented with either 5 or 50 g kg-1 printanor. As a reference, the commercially available fermented garlic kyolic was included (1.6 g kg-1 diet). Treatment with printanor demonstrated reduced body weight, coinciding with increased feces production and fecal fatty acids excretion. Printanor and kyolic treatment did not affect plasma lipids, markers of inflammation (serum amyloid A, serum-soluble intercellular adhesion molecule-1, and blood-leukocytes tumor necrosis factor-α (TNFα) production) and vascular activation (plasma von Willebrand factor (vWF)). As analyzed after 28 weeks of treatment, printanor and kyolic did not affect atherosclerotic lesion type, area or composition. Under conditions relevant to the human situation, the well-characterized and production-controlled garlic powder printanor does not display hypolipidemic, anti-inflammatory or anti-atherosclerotic properties. © 2004 Elsevier Ireland Ltd. All rights reserved. Chemicals / CAS: intercellular adhesion molecule 1, 126547-89-5; lipid, 66455-18-3; von Willebrand factor, 109319-16-6; apolipoprotein E3 (Leidein); Apolipoprotein E3; Apolipoproteins E; Intercellular Adhesion Molecule-1, 126547-89-5; Lipids; Serum Amyloid A Protein; Tumor Necrosis Factor-alpha; von Willebrand Factor
TNO Identifier
238186
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ISSN
00219150
Source
Atherosclerosis, 177(2), pp. 291-297.
Pages
291-297
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