Related Experiment Video

Updated: Aug 8, 2026

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction
08:41

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction

Published on: January 12, 2016

Vitamins C and E attenuate apoptosis, beta-adrenergic receptor desensitization, and sarcoplasmic reticular Ca2+

Fuzhong Qin1, Chen Yan, Ravish Patel

  • 1Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA. fqin@bu.edu

Free Radical Biology & Medicine
|May 9, 2006
PubMed

Insights

Antioxidant vitamins C and E reduced oxidative stress, myocyte apoptosis, and improved heart function in rabbits with heart failure after myocardial infarction. This suggests antioxidant therapy may benefit heart failure patients.

Area of Science:

  • Cardiology
  • Biochemistry
  • Molecular Biology

Background:

  • Oxidative stress is implicated in heart failure (HF) pathogenesis, contributing to ventricular remodeling and dysfunction.
  • The precise mechanisms by which oxidative stress affects HF progression remain incompletely understood.
  • Key cellular processes affected include myocyte apoptosis, beta-adrenergic receptor signaling, and calcium handling.

Purpose of the Study:

  • To investigate if combined antioxidant vitamins (C and E) can mitigate myocyte apoptosis, beta-adrenergic receptor desensitization, and sarcoplasmic reticular (SR) Ca2+ ATPase downregulation in HF post-myocardial infarction (MI).
  • To determine if these cellular effects correlate with improved left ventricular (LV) remodeling and function.
  • To assess the therapeutic potential of antioxidant vitamins in HF.

Main Methods:

  • Rabbits underwent myocardial infarction (MI) or sham operation, followed by 11 weeks of treatment with vitamin C (300 mg) and vitamin E (300 mg) or placebo.
  • Left ventricular (LV) function was assessed using fractional shortening and maximal rate of pressure rise (dP/dt).
  • Oxidative stress markers, apoptotic markers (Bcl-2, Bax, caspases), beta-adrenergic receptor sensitivity, and SR Ca2+ ATPase levels were quantified.

Main Results:

  • MI rabbits showed cardiac dilation, LV dysfunction, elevated oxidative stress, increased myocyte apoptosis, and impaired beta-adrenergic receptor and SR Ca2+ ATPase function.
  • Combined vitamin C and E treatment significantly reduced oxidative stress and myocyte apoptosis.
  • Antioxidant therapy normalized beta-adrenergic receptor sensitivity and SR Ca2+ ATPase function, attenuating LV remodeling and dysfunction.

Conclusions:

  • Combined antioxidant vitamin therapy effectively reduces oxidative stress and myocyte apoptosis in a rabbit model of heart failure post-MI.
  • This therapeutic approach preserves beta-adrenergic receptor sensitivity and SR Ca2+ ATPase function, leading to improved cardiac structure and function.
  • Antioxidant therapy represents a promising strategy for managing heart failure.

More Related Videos

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury07:23

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include: