Open AccessAntroquinonol, an active pure compound from Antrodia camphorate mycelium, modulates the development of atherosclerosis in a mouse carotid artery ligation model
Author(s) -
Tsai-Jung Lin,
Yun-Yi Lee,
Bieng-Hsian Tzeng,
Shih-Ping Yang,
C.L. Ho,
DuengYuan Hueng,
JiaMing Chang,
Kunlun Huang,
FuGong Lin,
Ann Chen,
Y. Hwu,
ShukMan Ka
Publication year - 2014
Publication title -
yīxué yánjiū zázhì/journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.176
H-Index - 12
eISSN - 2542-4939
pISSN - 1011-4564
DOI - 10.4103/1011-4564.131888
Subject(s) - platelet derived growth factor receptor , neointima , ligation , carotid arteries , smooth muscle , microbiology and biotechnology , chemistry , medicine , andrology , growth factor , biology , receptor , restenosis , stent
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