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

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Title:	Protective effects of magnolol against oxidized LDL-induced apoptosis in endothelial cells
Authors:	歐秀中(Hsiu-Chung Ou);周芬碧(Chou FP);許惠恒(Sheu WH);徐士蘭(Hsu SL);李文珍(Lee WJ)*
Contributors:	健康照護學院物理治療學系
Keywords:	Endothelium；OxLDL；Magnolol；Apoptosis；Mitochondrial membrane potential；Calcium homeostasis
Date:	2007-06
Issue Date:	2009-08-19 17:04:04 (UTC+8)
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.
Relation:	ARCHIVES OF TOXICOLOGY6(81):421~432
Appears in Collections:	[Department of Physical Therapy, Graduate Institute of Rehabilitation Science] Journal articles

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