Protective effects of magnolol against oxidized LDL-induced apoptosis in endothelial cells.

doi:10.1007/s00204-006-0172-3

CSMUIR > Medical College > The Institute of Biochemistry, Microbiology and Immunology > Journal Paper > Item 310902500/11571

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11571

Title:	Protective effects of magnolol against oxidized LDL-induced apoptosis in endothelial cells.
Authors:	Ou, HC Chou, FP Sheu, WH Hsu, SL Lee, WJ
Contributors:	中山醫學大學
Keywords:	Endothelium;OxLDL;Magnolol;Apoptosis;Mitochondrial membrane potential;Calcium homeostasis
Date:	2007
Issue Date:	2015-07-22T10:42:14Z (UTC)
ISSN:	0340-5761
Abstract:	Magnolol, a compound extracted from the Chinese medicinal herb Magnolia officinalis, has several biological effects. However, its protective effects against endothelial injury remain unclear. In this study, we examined whether magnolol prevents oxidized low density lipoprotein (oxLDL)-induced vascular endothelial apoptosis. Incubation of oxLDL with magnolol (2.5-20 microM) inhibited copper-induced oxidative modification via diene formation, thiobarbituric acid reactive substances (TBARS) assay and electrophoretic mobility assay. Apoptotic cell death as characterized by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) stain. We measured the production of reactive oxygen species (ROS) by using the fluorescent probe 2',7'-dichlorofluorescein acetoxymethyl ester (DCF-AM), and observed the activity of antioxidant enzymes. Furthermore, several apoptotic signaling pathways which showed NF-kappaB activation, increased cytosolic calcium, alteration of mitochondrial membrane potential, cytochrome c release and activation of caspase 3 were also investigated. We demonstrated that magnolol prevented the copper-induced oxidative modification of LDL. Magnolol attenuated the oxLDL-induced ROS generation and subsequent NF-kappaB activation. Furthermore, intracellular calcium accumulation and subsequent mitochondrial membrane potential collapse, cytochome c release and activation of caspase 3 caused by oxLDL were also inhibited by magnolol. Our results suggest that magnolol may have clinical implications in the prevention of atherosclerotic vascular disease through decreasing the oxLDL-induced ROS production.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11571 http://dx.doi.org/10.1007/s00204-006-0172-3
Relation:	Arch Toxicol. 2007 Jun;81(6):421-32.
Appears in Collections:	[The Institute of Biochemistry, Microbiology and Immunology ] Journal Paper

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