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Protective effects of magnolol against oxidized LDL‐induced cytotoxicity and adhesion molecule expression in endothelial cells
Author(s) -
Ou HsiuChung,
Wang JongShyan,
Sheu Wayne HueyHerng
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a316-b
Subject(s) - magnolol , enos , magnolia officinalis , reactive oxygen species , chemistry , cell adhesion molecule , microbiology and biotechnology , nitric oxide , apoptosis , adhesion , oxidative stress , endothelial dysfunction , biochemistry , pharmacology , nitric oxide synthase , biology , medicine , endocrinology , pathology , chromatography , alternative medicine , traditional chinese medicine , organic chemistry
Magnolol is a compound extracted from the Chinese medicinal herb Magnolia officinalis. Oxidized‐low density lipoprotein (ox‐LDL) induces endothelial dysfunction, accelerating pathogenesis of atherosclerosis. This study investigates how magnolol affects vascular endothelial function mediated by ox‐LDL. Copper‐induced oxidative modification, expressions of adhesion molecules and nitric oxide sythase (eNOS), production of reactive oxygen species (ROS), and apoptotic processes of endothelial cells were determined. Analytical results showed that (1) magnolol decreased extent of LDL oxidation induced by copper; (2) following treatment endothelial cells with magnolol, suppression of eNOS expression, enhancement of adhesion molecules expressions, and adhesion of THP1 cells to endothelial cells by ox‐LDL were ameliorated; and (3) magnolol inhibited ROS generation, intracellular calcium accumulation, mitochondrial membrane potential collapse, cytochome c release, and caspase‐3 activation induced by ox‐LDL, subsequently suppressing apoptosis of endothelial cells. Therefore, we conclude that magnolol may have clinical implications in the prevention of atherosclerotic vascular diseases