Related Experiment Video

Updated: May 30, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

Davallialactone protects against adriamycin-induced cardiotoxicity in vitro and in vivo

Sankarganesh Arunachalam1, Sun Young Kim, Sun Hwa Lee

  • 1Department of Pediatrics, Chonbuk National University Hospital, 634-18 Keumam-dong, Jeonju 561-712, Republic of Korea.

Journal of Natural Medicines
|August 23, 2011
PubMed

Insights

Davallialactone (DAVA) protects heart cells from Adriamycin (ADR)-induced damage. This mushroom extract reduces oxidative stress and apoptosis, offering potential for cancer patients undergoing ADR treatment.

Area of Science:

  • Cardiovascular Pharmacology
  • Natural Product Chemistry
  • Oncology Supportive Care

Background:

  • Adriamycin (ADR) is a vital chemotherapy agent, but its clinical use is limited by cardiotoxicity.
  • Oxidative stress and apoptosis in cardiac cells are key mechanisms underlying ADR-induced cardiomyopathy.
  • Davallialactone (DAVA), a mushroom-derived compound, exhibits antioxidant and free radical scavenging properties.

Purpose of the Study:

  • To investigate the cardioprotective effects of DAVA against ADR-induced oxidative stress and apoptosis in cardiac cells.
  • To compare DAVA's efficacy with N-acetylcysteine, a known antioxidant.
  • To evaluate DAVA's protective potential in an in vivo model of ADR-induced cardiotoxicity.

Main Methods:

  • Assessed cytotoxicity using MTT assay and crystal violet staining.
  • Measured reactive oxygen species (ROS) production via flow cytometry.
  • Analyzed protein expression (SOD, ERK, JNK, caspase-3, PARP) using Western blot.
  • Evaluated apoptosis through nuclear condensation and protein markers.
  • Conducted an in vivo study using an animal model of ADR-induced cardiomyopathy.

Main Results:

  • DAVA significantly enhanced the viability of doxorubicin-injured H9c2 cells.
  • DAVA inhibited ADR-induced ROS production, apoptosis, and the expression of Cu/Zn SOD and Mn-SOD.
  • DAVA suppressed the ADR-induced activation of the ERK and JNK signaling pathways.
  • In vivo studies showed DAVA significantly reduced cardiomyocyte lesions.

Conclusions:

  • Davallialactone demonstrates significant cardioprotective effects against Adriamycin-induced cardiotoxicity.
  • DAVA mitigates oxidative stress and apoptosis in cardiac cells, potentially via MAPK pathway modulation.
  • DAVA represents a promising therapeutic candidate for preventing cardiotoxicity in cancer patients treated with ADR.

More Related Videos

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...