Abstract
Background: Heart failure is one of the most important factors of death in industrialized countries. This study was performed to assess the anti-apoptotic effects of atorvastatin in isoproterenol induced experimental heart failure in rats.
Materials and Method: Fifty male Wistar rats were randomly divided into 5 groups of 10 animals each, including: 1-healthy control, 2-patient (heart failure) control, 3- patient treated with low dose of atorvastatin, 4- patient treated with moderate dose of atorvastatin, and 5- patient treated with high dose of atorvastatin. For inducing heart failure, isoproterenol was injected subcutaneously at a dose of 0.5 mg/kg daily for 10 days. Groups 1&2 received only normal saline (10 ml/kg). Groups 3-5 received atorvastatin at 5, 10 and 15 mg/kg respectively. All treatments were administered orally in 10 ml/kg normal saline solution, three weeks before isoproterenol injection and continued until the end of trial. Twenty-four hours after the last treatment, the rats were killed and histological sections from left ventricles were prepared through Tunnel staining method. Apoptotic cells were counted by the light microscope. Data were analyzed statistically by one-way ANOVA analysis.
Results: In group 2, isoproterenol treatment increased significantly in the numbers of apoptotic cells in comparison with healthy group (p<0.001). In groups 3-5 atorvastatin (5, 10 and 15 mg/kg) caused significant decrease (p<0.05, p<0.01 and p<0.001, respectively) in the numbers of apoptotic cells in comparison with group 2.
Conclusion: The results showed that atorvastatin may prevent isoproterenol induced cardiomyocytes apoptotosis in the rats.
Keywords
Fulltext
The full text of this article is available on the PDF file.
References
-
1.
The References of this article are available on the PDF file.
Copyright
© 2011, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.