Probucol Prevents Atrial Remodeling by Inhibiting Oxidative Stress and TNF-α/NF-κB/TGF-β Signal Transduction Pathway in Alloxan-Induced Diabetic Rabbits.

Probucol Prevents Atrial Remodeling Introduction Diabetes mellitus (DM) is an independent risk factor for atrial fibrillation (AF). However, the underlying mechanisms for the increased propensity for AF in the setting of DM and the potential effects of probucol on atrial remodeling remain unclear. M...

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Publicado en:Journal of Cardiovascular Electrophysiology Vol. 26; no. 2; pp. 211 - 223
Autores principales: FU, HUAYING, LI, GUANGPING, LIU, CHANGLE, LI, JIAN, WANG, XINGHUA, CHENG, LIJUN, LIU, TONG
Formato: diagnostic images pictorial research tables/charts tracings Journal Article
Publicado: Wiley-Blackwell Feb2015
Acceso en línea:Ver este registro en EBSCOhost
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      pub: Wiley-Blackwell
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        atl: Probucol Prevents Atrial Remodeling by Inhibiting Oxidative Stress and TNF-α/NF-κB/TGF-β Signal Transduction Pathway in Alloxan-Induced Diabetic Rabbits.
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          FU, HUAYING
          LI, GUANGPING
          LIU, CHANGLE
          LI, JIAN
          WANG, XINGHUA
          CHENG, LIJUN
          LIU, TONG
        affil: Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University
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        subj:
          Phenols Administration and Dosage
          Oxidative Stress
          Tumor Necrosis Factor Drug Effects
          NF-kappa B Drug Effects
          Growth Substances Drug Effects
          Signal Transduction Drug Effects
          Heart Atrium Drug Effects
          Animal Studies
          Rabbits
          Descriptive Statistics
          Random Assignment
          Heterocyclic Compounds Administration and Dosage
          Diabetes Mellitus Chemically Induced
          Atrial Fibrillation Risk Factors
          Diabetes Mellitus Complications
          Malondialdehyde Analysis
          Superoxide Dismutase Analysis
          Oxidoreductases Analysis
          Blotting, Western
          China
          Hemodynamics
          Electrophysiology
          Echocardiography
          Tissue Culture Techniques
          Data Analysis Software
          Polymerase Chain Reaction
          Fisher's Exact Test
          One-Way Analysis of Variance
          Funding Source
      ab: Probucol Prevents Atrial Remodeling Introduction Diabetes mellitus (DM) is an independent risk factor for atrial fibrillation (AF). However, the underlying mechanisms for the increased propensity for AF in the setting of DM and the potential effects of probucol on atrial remodeling remain unclear. Methods and Results Eighty Japanese rabbits were randomly assigned to normal/control group (Control, n = 20), alloxan-induced diabetic group (DM, n = 20), probucol-treated group (Control-P, n = 20), and probucol-treated diabetic group (DM-P, n = 20). Rabbits in the DPR and CPR groups were orally administered probucol (1,000 mg/day) for 8 weeks. Serum and left atrial tissue malonaldehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO), and catalase (CAT) levels were assessed. Isolated Langendorff perfused rabbit hearts were prepared to evaluate atrial refractory effective period (AERP) and its dispersion (AERPD), interatrial conduction time (IACT), and vulnerability to AF. Atrial interstitial fibrosis was also evaluated. The mRNA expression levels of TNF-α and TLR4 were analyzed. The protein expressions of NF-κB, HSP70, TGF-β, and ERK in left atrial tissue were analyzed by Western blot. Probucol administration decreased the inducibility of AF in diabetic rabbits and attenuated atrial interstitial fibrosis. The DM-P rabbits exhibited significant alleviation of oxidative stress, evidenced by reduced serum and tissue MDA, compared with diabetic rabbits. Moreover, NF-κB, TGF-β, and HSP70 protein expression and TNF-α mRNA expression were significantly downregulated by probucol treatment in alloxan-induced diabetic rabbits. Conclusions Probucol prevents atrial remodeling and suppresses AF development in alloxan-induced diabetic rabbits. Its inhibitory effects on oxidative stress, NF-κB, TGF-β, and TNF-α overexpression may contribute to its antiremodeling effects.
      pubtype: Academic Journal
      doctype:
        diagnostic images
        pictorial
        research
        tables/charts
        tracings
        Journal Article
      ougenre: Article
    language: English
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