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TPEN prevents rapid pacing-induced calcium overload and nitration stress in HL-1 myocytes

Shusen Yang1, Wenjing Xu1, Zengxiang Dong1

  • 1Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Cardiovascular Therapeutics
|May 15, 2015
PubMed
Abstract

Insights

TPEN reduces nitration stress and calcium overload in atrial cells during simulated atrial fibrillation (AF). This finding suggests TPEN may protect against AF-related cellular damage.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Atrial fibrillation (AF) is a common arrhythmia with limited treatment options.
  • Nitration stress is increasingly recognized as a factor in AF development.
  • Existing antiarrhythmic drugs have efficacy limitations and side effects.

Purpose of the Study:

  • To investigate the potential antinitration effects of TPEN on atrial myocytes.
  • To assess TPEN's protective role against nitration stress and AF-like conditions.
  • To evaluate TPEN's impact on cellular damage markers in AF models.

Main Methods:

  • Utilized a rapid pacing HL-1 cell model to simulate AF.
  • Assessed electrophysiological and structural changes using patch clamp and TEM.
  • Examined TPEN's effects on cell viability, apoptosis, and protein nitration via MTT, TUNEL, confocal microscopy, and Western blot.

Main Results:

  • TPEN significantly ameliorated ONOO(-) induced cell damage and reduced cell viability.
  • TPEN inhibited calcium overload caused by rapid pacing and ONOO(-) stimulation.
  • TPEN prevented protein nitration and reduced apoptosis in paced and ONOO(-) treated cells.

Conclusions:

  • TPEN demonstrates protective antinitration effects on atrial myocytes.
  • TPEN mitigates calcium overload and apoptosis under AF-like conditions.
  • TPEN shows potential as a therapeutic agent for AF by reducing nitration stress.
Keywords:
ApoptosisAtrial fibrillationNitration stressONOO −TPEN

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