Probucol prevents atrial ion channel remodeling in an alloxaninduced diabetes rabbit model

Huaying Fu; Guangping Li; Changle Liu; Jian Li; Lijun Cheng; Wansong Yang; Gary Tse; Jichao Zhao; Tong Liu

doi:10.18632/oncotarget.13339

Probucol prevents atrial ion channel remodeling in an alloxaninduced diabetes rabbit model

Huaying Fu
, Guangping Li
, Changle Liu
, Jian Li
, Lijun Cheng
, Wansong Yang
, Gary Tse
, Jichao Zhao
, Tong Liu

Research output: Contribution to journal › Article › peer-review

17 Citations (Scopus)

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, I_Ca,L, I_Na and action potential durations (APDs) were measured in cardiomyocytes isolated from the left atria in the four groups, respectively. In the DM group, increased I_ca,L and decreased I_Na 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.

Original language	English
Pages (from-to)	83850-83858
Number of pages	9
Journal	Oncotarget
Volume	7
Issue number	51
DOIs	https://doi.org/10.18632/oncotarget.13339
Publication status	Published - 2016
Externally published	Yes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Alloxan-induced diabetes
Atrial fibrillation
Atrial ionic remodeling
Calcium current
Diabetes mellitus
Pathology Section

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10.18632/oncotarget.13339

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title = "Probucol prevents atrial ion channel remodeling in an alloxaninduced 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.",

keywords = "Alloxan-induced diabetes, Atrial fibrillation, Atrial ionic remodeling, Calcium current, Diabetes mellitus, Pathology Section",

author = "Huaying Fu and Guangping Li and Changle Liu and Jian Li and Lijun Cheng and Wansong Yang and Gary Tse and Jichao Zhao and Tong Liu",

note = "Funding Information: This work was supported by grants (30900618, 81270245, 81570298 to T.L.) from the National Natural Science Foundation of China, Tianjin Natural Science Foundation (16JCYBJC25000 to H.F., 16JCZDJC34900 to T.L.), the Croucher Foundation of Hong Kong (Diabetes Project Grant and Clinical Assistant Professorship to G.T.) and the Health Research Council of New Zealand (J.Z.).",

year = "2016",

doi = "10.18632/oncotarget.13339",

language = "English",

volume = "7",

pages = "83850--83858",

number = "51",

}

TY - JOUR

T1 - Probucol prevents atrial ion channel remodeling in an alloxaninduced diabetes rabbit model

AU - Fu, Huaying

AU - Li, Guangping

AU - Liu, Changle

AU - Li, Jian

AU - Cheng, Lijun

AU - Yang, Wansong

AU - Tse, Gary

AU - Zhao, Jichao

AU - Liu, Tong

N1 - Funding Information: This work was supported by grants (30900618, 81270245, 81570298 to T.L.) from the National Natural Science Foundation of China, Tianjin Natural Science Foundation (16JCYBJC25000 to H.F., 16JCZDJC34900 to T.L.), the Croucher Foundation of Hong Kong (Diabetes Project Grant and Clinical Assistant Professorship to G.T.) and the Health Research Council of New Zealand (J.Z.).

PY - 2016

Y1 - 2016

N2 - 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.

AB - 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.

KW - Alloxan-induced diabetes

KW - Atrial fibrillation

KW - Atrial ionic remodeling

KW - Calcium current

KW - Diabetes mellitus

KW - Pathology Section

UR - https://www.scopus.com/pages/publications/85007452370

U2 - 10.18632/oncotarget.13339

DO - 10.18632/oncotarget.13339

M3 - Article

C2 - 27863381

AN - SCOPUS:85007452370

VL - 7

SP - 83850

EP - 83858

JO - Oncotarget

JF - Oncotarget

IS - 51

ER -

Probucol prevents atrial ion channel remodeling in an alloxaninduced diabetes rabbit model

Abstract

UN SDGs

Keywords

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