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ORIGINAL ARTICLE
Year : 2014  |  Volume : 34  |  Issue : 2  |  Page : 56-61

Antroquinonol, an active pure compound from Antrodia camphorate mycelium, modulates the development of atherosclerosis in a mouse carotid artery ligation model


1 Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, Republic of China
2 Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan, Republic of China
3 Department of Medicine, Division of Cardiology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China
4 Department of Neurological Surgery, Tri-Service General Hospital; Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan, Republic of China
5 Department of Animal Pharmacology, Development Center for Biotechnology, Taipei, Taiwan, Republic of China
6 School of Public Health, National Defense Medical Center, Taipei, Taiwan, Republic of China
7 Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China
8 Institute of Physics, Academia Sinica, Nan-Kang, Taipei, Taiwan, Republic of China

Correspondence Address:
Prof. Shuk-Man Ka
Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, No. 161, Section 6, Min-Quan E. Road, Taipei, Taiwan
Republic of China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1011-4564.131888

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Background: Antroquinonol (Antroq) is an active component of Antrodia camphorate. The present study was to validate the preventive effects of Antroq in an atherosclerosis model. Materials and Methods: We examined Antroq inhibitory effect on rat aortic smooth muscle cell proliferation and migration and evaluated its effect on neointima formation and inflammation in mouse carotid artery ligation (CAL). Results: Our data show that Antroq [1] inhibited the proliferation (Antroq [3.0 μg/ml] + PDGF 41.7 ± 7.3%, vehicle + PDGF 134.5 ± 7.3%) (p<0.005) and migration (6h: Antroq [3.0 μg/ml] + PDGF 0.9 ± 0.3%, vehicle + PDGF 25.0 ± 3.4%; 12h: Antroq [3.0 μg/ml] + PDGF 4.0 ± 1.6%, vehicle + PDGF 40.5 ± 2.2%; 24h: Antroq [3.0 μg/ml] + PDGF 14.2 ± 3.0%, vehicle + PDGF 59.8 ± 3.3%) (each, p<0.005) of the cultured smooth muscle cells, [2] prevented neointima formation and reduced N/M ratios in CAL mice (900 μm: Antroq + CAL 0.8 ± 0.3, CAL 3.5 ± 1.1; 800 μm: Antroq + CAL 0.6 ± 0.2, CAL 3.5 ± 0.7; 700 μm: Antroq + CAL 0.7 ± 0.2, CAL 3.8 ± 0.4; 600 μm: Antroq + CAL 0.9 ± 0.2, CAL 3.8 ± 0.9; 500 μm: Antroq + CAL 1.3 ± 0.4, CAL 3.9 ± 0.8; 400 μm: Antroq + CAL 1.5 ± 0.5, CAL 4.0 ± 1.0; 300 μm: Antroq + CAL 1.8 ± 0.6, CAL 3.5 ± 0.6; 200 μm: Antroq + CAL 2.3 ± 0.6, CAL 4.6 ± 1.1) (each, p<0.01), [3] and prevented inflammatory processes and matrix accumulation/fibrosis in the CAL mice. Conclusions: Our data may be useful in developing new and practical strategy for the prevention of atherosclerosis based on the pathogenesis of the disorder.


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