title: Attenuation of oxidative stress and cardiac dysfunction by bisoprolol in an animal model of dilated cardiomyopathy.
abstract: Oxidative stress is an important susceptibility factor for dilated cardiomyopathy. We have investigated the effects of bisoprolol, a beta1-selective adrenoceptor blocker, on oxidative stress and the development of cardiac dysfunction in a model of dilated cardiomyopathy. Male TO-2 and control hamsters at 8 weeks of age were treated with bisoprolol (5 mg/kg per day) or vehicle for 4 weeks. Treatment with bisoprolol prevented the progression of cardiac dysfunction in TO-2 hamsters. This drug did not affect the increase in NADPH oxidase activity but prevented the reduction in activity and expression of mitochondrial manganese-dependent superoxide dismutase as well as the increases in the concentrations of interleukin-1beta and tumor necrosis factor-alpha in the left ventricle of TO-2 hamsters. Attenuation of the development of cardiac dysfunction by bisoprolol may thus result in part from normalization of the associated increases in the levels of oxidative stress and pro-inflammatory cytokines in the left ventricle.
authors.affiliation: Department of Human Functional Genomics, Life Science Research Center, Mie University, Tsu, Japan. saho@gene.mie-u.ac.jp
authors.forename: Sahoko
authors.initials: S
authors.lastname: Ichihara
authors.forename: Yoshiji
authors.initials: Y
authors.lastname: Yamada
authors.forename: Gaku
authors.initials: G
authors.lastname: Ichihara
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kanazawa
authors.forename: Katsunori
authors.initials: K
authors.lastname: Hashimoto
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Kato
authors.forename: Aya
authors.initials: A
authors.lastname: Matsushita
authors.forename: Shinji
authors.initials: S
authors.lastname: Oikawa
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokota
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Iwase
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017298:Bisoprolol / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002311:Cardiomyopathy, Dilated / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006224:Cricetinae; D004195:Disease Models, Animal; D004452:Echocardiography; D005355:Fibrosis / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000031:analogs & derivatives / Q000378:metabolism; D006333:Heart Failure / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects; D007375:Interleukin-1 / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism; D016277:Ventricular Function, Left
chemical_list: D000447:Aldehydes; D000975:Antioxidants; D007375:Interleukin-1; D007527:Isoenzymes; D014409:Tumor Necrosis Factor-alpha; C002744:3-nitrotyrosine; D014443:Tyrosine; D013482:Superoxide Dismutase; D019255:NADPH Oxidases; D005978:Glutathione; C027576:4-hydroxy-2-nonenal; D017298:Bisoprolol