title: (-)-Epicatechin Attenuates Degradation of Mouse Oxidative Muscle Following Hindlimb Suspension.
abstract: The purpose of this study was to conduct a 14-day hindlimb suspension (HS) with and without (-)-epicatechin supplementation to determine whether (-)-epicatechin treatment can attenuate the loss in muscle degradation, angiogenesis, and mitochondrial signaling in oxidative skeletal muscle. Adult mice were randomized into 3 groups: (a) control (C); (b) HS with vehicle (HS-V); and (c) HS with (-)-epicatechin (HS-(-)-Epi). Animals in the HS-(-)-Epi group received (-)-epicatechin (1.0 mg · kg(-1) of body mass) twice daily through oral gavage. For markers related to muscle degradation, the HS-V group had significantly higher protein expression compared with the control and HS-(-)-Epi groups. Moreover, protein expression for myosin heavy chain type I was significantly reduced by approximately 45% in the HS-V group compared with the control and HS-(-)-Epi groups. In addition, capillarity contact and capillary-to-fiber ratio were significantly higher in the HS-(-)-Epi group compared with the HS-V group. Furthermore, protein expression for thrombospondin-1 was significantly higher in HS-V group compared with the control and HS-(-)-Epi groups. Hindlimb suspension also significantly reduced protein expression for mitochondrial signaling compared with the control and HS-(-)-Epi groups. These findings suggest that (-)-epicatechin supplementation attenuates degradation in oxidative muscles after HS.
authors.affiliation: 1College of Medicine, Dankook University, Cheonan-si, Republic of Korea; 2Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan; 3Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan; and 4Integrative Physiology of Exercise Laboratory, Department of Health Care Sciences, Eugene Applebaum College of Pharmacy & Health Sciences, Wayne State University, Detroit, Michigan.
authors.forename: Icksoo
authors.initials: I
authors.lastname: Lee
authors.forename: Maik
authors.initials: M
authors.lastname: Hüttemann
authors.forename: Moh H
authors.initials: MH
authors.lastname: Malek
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects; D000818:Animals; D002196:Capillaries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D002197:Capillary Action / Q000187:drug effects; D002392:Catechin / Q000494:pharmacology*; D019417:Hindlimb Suspension / Q000009:adverse effects / Q000502:physiology; D008297:Male; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D018995:Myosin Heavy Chains / Q000378:metabolism*; D024461:Myosin Type I / Q000378:metabolism*; D018919:Neovascularization, Physiologic / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D019700:Thrombospondin 1 / Q000378:metabolism
chemical_list: D019700:Thrombospondin 1; C585483:Thbs1 protein, mouse; D002392:Catechin; D024461:Myosin Type I; D018995:Myosin Heavy Chains