Related Experiment Video
Updated: Jun 11, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Naproxen aggravates doxorubicin-induced cardiomyopathy in rats
Rahila Ahmad Pathan1, Bhulan Kumar Singh, K K Pillai
1Department of Pharmacology, Faculty of Pharmacy, Hamdard University, Hamdard Nagar, New Delhi 110062, India.
Background:
The repercussion of the heated dispute on cyclooxygenase-2 (COX-2) selective nonsteroidal anti-inflammatory drugs (NSAIDs) led to the national and international withdrawal of several of the recently introduced coxibs. Further debate and research have highlighted risks of the classical NSAIDs too. There is much controversy about the cardiovascular safety of a nonselective NSAID naproxen (NAP) and its possible cardioprotective effect.
Objectives:
The study was undertaken to determine the cardiovascular effects of NAP on doxorubicin-induced cardiomyopathy in rats.
Materials And Methods:
Male albino rats received a single i.p. injection of normal saline (normal control group) and doxorubicin (DOX) 15 mg/kg (toxic control group). Naproxen was administered alone (50 mg/kg/day, p.o.) and in combination with DOX and DOX + trimetazidine (TMZ) (10 mg/kg/day, p.o.) for 5 days after 24 h of DOX treatment. DOX-induced cardiomyopathy was assessed in terms of increased activities of serum lactate dehydrogenase (LDH), tissue thiobarbituric acid reactive substances (TBARS) and decreased activities of myocardial glutathione, superoxide dismutase and catalase, followed by transmission electron microscopy of the cardiac tissue.
Results:
Doxorubicin significantly increased oxidative stress as evidenced by increased levels of LDH and TBARS and decreased antioxidant enzymes levels. Both biochemical and electron microscopic studies revealed that NAP itself was cardiotoxic and aggravated DOX-induced cardiomyopathy and abolished the protective effect of TMZ in rats.
Conclusions:
This study indicates that NAP has the potential to worsen the situation in patients with cardiovascular disease. Therefore, it should be used cautiously in patients with compromised cardiac function.
Insights
Naproxen (NAP), a nonselective NSAID, was found to be cardiotoxic in rats, worsening doxorubicin-induced cardiomyopathy. This suggests caution when using naproxen in patients with cardiovascular disease.
Area of Science:
- Cardiology
- Pharmacology
- Toxicology
Background:
- Debate surrounds the cardiovascular safety of nonselective NSAIDs, specifically naproxen (NAP).
- Previous research highlighted risks associated with NSAIDs, including coxibs and classical agents.
- The potential cardioprotective effect of naproxen remains controversial.
Purpose of the Study:
- To investigate the cardiovascular effects of naproxen in a rat model of doxorubicin-induced cardiomyopathy.
- To assess naproxen's impact on cardiac function and oxidative stress markers.
Main Methods:
- Male rats received doxorubicin (DOX) to induce cardiomyopathy.
- Naproxen was administered alone or in combination with DOX and trimetazidine (TMZ).
- Cardiomyopathy was evaluated using biochemical markers (LDH, TBARS, antioxidant enzymes) and electron microscopy.
Main Results:
- Doxorubicin significantly increased oxidative stress markers and decreased antioxidant enzyme levels.
- Naproxen alone demonstrated cardiotoxicity and exacerbated DOX-induced cardiomyopathy.
- Naproxen abolished the protective effects of trimetazidine against DOX-induced cardiac damage.
Conclusions:
- Naproxen exhibits cardiotoxic potential and can worsen pre-existing cardiovascular conditions.
- Cautious use of naproxen is recommended for patients with compromised cardiac function.
- Further research is warranted to elucidate the cardiovascular risks associated with naproxen.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Heart Failure Drugs: Inotropic Agents
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
