Anti-atherosclerotic effect of cilostazol in apolipoprotein-E knockout mice
| Autor: | Ayako Hashimoto, Takashi Imaizumi, Toyoki Mori, Hideki Ito, Goro Miyakoda, Hiromichi Takase, Reiko Okutsu, Yoshimi Hirose |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Apolipoprotein E
Male medicine.medical_specialty Aging Apolipoprotein B Phosphodiesterase Inhibitors Phosphodiesterase 3 Tetrazoles Vascular Cell Adhesion Molecule-1 Monocytes Lesion chemistry.chemical_compound Mice Apolipoproteins E Internal medicine Drug Discovery medicine Animals Triglycerides Mice Knockout biology Chemistry Cholesterol Cholesterol HDL Atherosclerosis Lipids Cilostazol Endocrinology Knockout mouse biology.protein medicine.symptom Lipoprotein medicine.drug |
| Zdroj: | Arzneimittel-Forschung. 57(4) |
| ISSN: | 0004-4172 |
| Popis: | To investigate whether cilostazol (CAS 73963-72-1), a selective phosphodiesterase 3 inhibitor, reduces the progression of atherogenic diet-induced atherosclerosis, cilostazol was orally administered twice a day for 4 weeks to male apolipoprotein-E knockout (ApoE KO) mice. In serial sections of the aortic root, the atherosclerotic lesion ratios in the cilostazol-treated groups (32.5 +/- 3.3% for 100 mg/kg, 29.0 +/- 2.9% for 300 mg/kg) were significantly and dose-dependently smaller than that of the control group (40.2 +/- 3.7%). Cilostazol also significantly reduced the expression of vascular cell adhesion molecule-1 (VCAM-1) and monocyte/macrophage accumulation in the aortic root and increased high-density lipoprotein(HDL) cholesterol levels in plasma. These results suggest that cilostazol suppresses the progression of atherosclerosis in ApoE KO mice by inhibiting adhesionand infiltration of monocytes and reducing cholesterol accumulation in atherosclerotic lesion. |
| Databáze: | OpenAIRE |
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