title: Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model.
abstract: Diabetes mellitus (DM) increases the risk of developing atrial fibrillation (AF), but the molecular mechanisms of diabetes-induced atrial remodeling processes have not been fully characterized. The aim of this study was to examine the mechanisms underlying atrial ion channel remodeling in alloxan-induced diabetes model in rabbits. A total of 40 Japanese rabbits were randomly assigned to a control group (C), alloxan-induced diabetic group (DM), probucol-treated control group (Control-P), and probucol-treated diabetic group (DM-P). Using whole-cell voltage-clamp techniques, ICa,L, INa and action potential durations (APDs) were measured in cardiomyocytes isolated from the left atria in the four groups, respectively. In the DM group, increased Ica,L and decreased INa currents were reflected in prolonged APD90 and APD50 values. These changes were reversed in the DM-P group. In conclusion, probucol cured AF by alleviating the ion channel remodeling of atrial myocytes in the setting of diabetes and the promising therapeutic potential of anti-oxidative compounds in the treatment of AF warrants further study.
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Huaying
authors.initials: H
authors.lastname: Fu
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Guangping
authors.initials: G
authors.lastname: Li
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Changle
authors.initials: C
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Lijun
authors.initials: L
authors.lastname: Cheng
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Wansong
authors.initials: W
authors.lastname: Yang
authors.affiliation: Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, SAR, P.R. China.|Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, SAR, P.R. China.
authors.forename: Gary
authors.initials: G
authors.lastname: Tse
authors.affiliation: Auckland Bioengineering Institute, The University of Auckland, New Zealand.
authors.forename: Jichao
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Department of Cardiology, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, People's Republic of China.
authors.forename: Tong
authors.initials: T
authors.lastname: Liu
mesh_terms: D000200:Action Potentials; D000496:Alloxan; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D001281:Atrial Fibrillation / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D064752:Atrial Remodeling / Q000187:drug effects*; D015415:Biomarkers / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000139:chemically induced / Q000175:diagnosis / Q000188:drug therapy*; D006325:Heart Atria / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D007473:Ion Channels / Q000187:drug effects* / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011341:Probucol / Q000494:pharmacology*; D011817:Rabbits; D013997:Time Factors
chemical_list: D000889:Anti-Arrhythmia Agents; D000975:Antioxidants; D015415:Biomarkers; D007473:Ion Channels; D000496:Alloxan; D011341:Probucol
keywords: Pathology Section; alloxan-induced diabetes; atrial fibrillation; atrial ionic remodeling; calcium current; diabetes mellitus