Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license

Authors

1 Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran.

2 Corresponding Author, Department of Physical Education and Sport Sciences, Marand Branch, Islamic Azad University, Marand, Iran.

3 Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Abstract

Introduction: Doxorubicin (DOX) is an effective chemotherapy treatment for various cancers, but its use has been restricted due to cardiotoxicity effects. Studies about the protective effect of High-Intensity Interval Training (HIIT) against DOX-induced cardiotoxicity and its mechanisms are rare. This study aimed to investigate the protective effect of HIIT against the DOX-induced cardiotoxicity on the level of miR-499 expression which is widely expressed under the physiological conditions in the cardiomyocytes.
Methods: Twenty-four male Wistar rats were randomly assigned into four groups (n=6/group) including DOX (20 mg/kg body weight), HIIT (eight weeks, and seven 4-minutes sets of intervals at 80%–90% of VO2max interspersed with 3 minutes periods at 65%–75% of VO2max), HIIT+DOX and Control groups. The mRNA expression level was determined using the RT-PCR method. One-way analysis of variance followed by Tukey's post hoc test was used for statistical analysis of data (α<0.05).
Results: The results showed that DOX-induction significantly increased the MIR-499 expression in the left ventricular tissue of the rats’ heart (P<0.05). Also, the expression level of MIR-499 was increased after exercise, but this difference was not statistically significant. Exercise before the DOX-induction also led to a significant reduction of MIR-499 expression in the HIIT+ DOX group compared with the DOX group (P<0.05).
Conclusion: Therefore, performing HIIT before DOX induction can reduce the changes in MIR-499 expression caused by DOX. Therefore, HIIT could be a proper strategy for protecting the heart against DOX-induced cardiotoxicity by reducing MIR-499 expression.

Keywords

Main Subjects

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