Cardioprotective effect of ritonavir, an antiviral drug, in isoproterenol induced myocardial necrosis: a new therapeutic implication

Ritonavir is a HIV protease inhibitor. In addition to its antiviral effect, Ritonavir directly inhibits the insulin-regulated glucose transporter GLUT4 and blocks glucose entry into fat and muscle cells. However, the effect of Ritonavir on cardiac GLUT4 inhibition during myocardial necrosis is not i...

Full description

Saved in:
Bibliographic Details
Published in:Journal of translational medicine 2013-03, Vol.11 (1), p.80-80, Article 80
Main Authors: Gupta, Prachi, Kanwal, Abhinav, Putcha, Uday Kumar, Bulani, Yogesh, Sojitra, Bhavesh, Khatua, Tarak Nath, Kuncha, Madhusudana, Banerjee, Sanjay Kumar
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Antioxidants - metabolism
Antioxidants - pharmacology
Body Weight
Cardiomyopathies - chemically induced
Cardiomyopathies - drug therapy
Cardiotonic Agents - therapeutic use
Cardiovascular diseases
Comparative analysis
Complications and side effects
Dextrose
Dosage and administration
Drug therapy
Glucose
Glucose Transporter Type 4 - metabolism
Health aspects
Heart attack
Heart attacks
Human immunodeficiency virus
Industrial research
Isoproterenol - adverse effects
Male
Mice
Necrosis
Necrosis - chemically induced
Necrosis - drug therapy
Nitric oxide
Nitric Oxide - metabolism
Nutrition
Oxidative Stress
Patient outcomes
Pharmacology
Phlorhizin - pharmacology
Proteases
Risk factors
Ritonavir
Ritonavir - therapeutic use
Rodents
Statistical analysis
Studies
Thiobarbituric Acid Reactive Substances - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Ritonavir is a HIV protease inhibitor. In addition to its antiviral effect, Ritonavir directly inhibits the insulin-regulated glucose transporter GLUT4 and blocks glucose entry into fat and muscle cells. However, the effect of Ritonavir on cardiac GLUT4 inhibition during myocardial necrosis is not investigated. In the present study, we evaluated the role of Ritonavir in isoproterenol-induced myocardial necrosis in vivo and compared the effect with Phlorizin, a nonslective SGLTs inhibitor. Isoproterenol (ISO) (150 mg/kg/day, i.p for 2 consecutive days) was administered to mice to cause myocardial necrosis. Phlorizin (400 mg/kg/day i.p twice daily for 2 days) and Ritonavir (10 mg/kg/day i.p twice daily for 2 days) were administered in two different groups of mice before isoproterenol administration. Isoproterenol (ISO) (150 mg/kg/day, i.p for 2 consecutive days) administration caused significant (p 
ISSN:1479-5876
1479-5876
DOI:10.1186/1479-5876-11-80