Pharmacology in Health Food: Metabolism of Quercetin In Vivo and Its Protective Effect Against Arteriosclerosis

Journal of Pharmacological Sciences

Kazuo Minakuchi³  Yasumasa Ikeda⁵  Masanori Yoshizumi²  Shuhei Tomita⁵  Yoshitaka Kihira⁵  Toshiaki Tamaki⁵  Junji Terao¹  Keisuke Ishizawa⁴  Yoshichika Kawai¹  Koichiro Tsuchiya⁴ 

[1] Department of Food Science, Institute of Health Bioscience, The University of Tokushima Graduate School, Japan;Department of Pharmacology, Nara Medical University School of Medicine, Japan;Department of Clinical Pharmacy, Institute of Health Bioscience, The University of Tokushima Graduate School, Japan;Department of Medical Pharmacology, Institute of Health Bioscience, The University of Tokushima Graduate School, Japan;Department of Pharmacology, Institute of Health Bioscience, The University of Tokushima Graduate School, Japan

关键词: quercetin glucuronide;    cardiovascular disease;    vascular smooth muscle cell;    health food;   

DOI  :  10.1254/jphs.10R38FM

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(46)Cited-By(33)Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor–induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II–induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders.

【 授权许可】

Unknown