title: Cardioprotective effect of resveratrol on lipopolysaccharide-induced oxidative stress in rat.
abstract: Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of Gram-negative bacteria, which induces a deleterious effect on several organs, including the heart, eventually leading to septic shock and death. Endotoxemia-induced cardiotoxicity is characterized by disturbed intracellular redox balance, excessive reactive oxygen species (ROS) accumulation, inducing DNA, protein, and membrane lipid damage. Resveratrol (trans-3,5,4' trihydroxystilbene; RVT) is a phytoalexin polyphenol that exhibits antioxidant and -inflammatory properties. We investigated the putative effect of a subacute treatment with this natural compound on LPS-induced cardiotoxicity in the rat. We found that resveratrol counteracted LPS-induced lipoperoxidation and decreased superoxide dismutase (SOD) activity, but had no effect on the LPS-induced decrease in catalase (CAT) nor on the increase in peroxidase (POD) activity. Resveratrol also reversed LPS-induced myocardial nitric oxide (NO) elevation. More important, LPS-induced iron depletion from plasma to the myocardial compartment was abolished upon resveratrol treatment. All these data suggest that resveratrol is capable of alleviating LPS-induced cardiotoxicity, and that its mode of action may involve iron-shuttling proteins.
authors.affiliation: Laboratoire de Biosurveillance de l'Environnement, Faculté des Sciences de Bizerte, Zarzouna, Tunisie. sebaihichem@yahoo.com
authors.forename: Hichem
authors.initials: H
authors.lastname: Sebai
authors.forename: Mamane
authors.initials: M
authors.lastname: Sani
authors.forename: Ezzedine
authors.initials: E
authors.lastname: Aouani
authors.forename: Néziha
authors.initials: N
authors.lastname: Ghanem-Boughanmi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000037:antagonists & inhibitors / Q000378:metabolism; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000150:complications / Q000473:pathology / Q000517:prevention & control*; D006321:Heart / Q000187:drug effects; D006331:Heart Diseases / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000975:Antioxidants; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D013267:Stilbenes; D009569:Nitric Oxide; D002374:Catalase; D009195:Peroxidase; D013482:Superoxide Dismutase; D000077185:Resveratrol