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Keishi‐bukuryo‐gan preserves the endothelium dependent relaxation of thoracic aorta in cholesterol‐fed rabbit by limiting superoxide generation
Author(s) -
Sekiya Nobuyasu,
Goto Hirozo,
Tazawa Kenji,
Oida Shoko,
Shimada Yutaka,
Terasawa Katsutoshi
Publication year - 2002
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.945
Subject(s) - lipid peroxide , endothelium , chemistry , radical , cholesterol , endocrinology , medicine , in vivo , vasodilation , superoxide , thoracic aorta , biochemistry , superoxide dismutase , aorta , biology , oxidative stress , enzyme , microbiology and biotechnology
Formerly, we have reported that keishi‐bukuryo‐gan prevents the progression of atherosclerosis in cholesterol‐fed rabbits and inhibits the free radical‐induced RBC haemolysis in rats. The present study was performed to investigate how keishi‐bukuryo‐gan (KBG) inhibits the early stage of atherosclerosis. Plasma lipid concentration and hydroxyl radical generation during respiratory burst in neutrophils were evaluated at the start and end of the study. The protective effect of KBG against endothelium disorder due to hypercholesterolaemia was examined. Twelve male Japanese white rabbits (2 kg body weight) were divided into two groups. Group A ( n = 6) was fed standard rabbit chow containing 1% cholesterol for 4 weeks. Group B ( n = 6) was fed standard rabbit chow containing 1% cholesterol and 1% KBG for 4 weeks. In the plasma lipid concentration, only the lipid peroxide concentration of group A was significantly higher than that of group B. At the end of the study, DMPO‐OH, the spin‐trapped adduct of hydroxyl radicals generated by neutrophils, was increased in both groups, and this increase was marked in group B. Endothelium‐dependent vasodilatation by acetylcholine increased significantly in group B compared with group A. Thus, KBG protects the vascular endothelium function by its antioxidative effect and by inhibiting the release of free radicals from neutrophils in vivo . Copyright © 2002 John Wiley & Sons, Ltd.