High-Intensity Interval Training Improves Cardiac Function by miR-206 Dependent HSP60 Induction in Diabetic Rats

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  • Maryam Delfan
  • Raheleh Amadeh Juybari
  • Sattar Gorgani-Firuzjaee
  • Nielsen, Jens Høiriis
  • Neda Delfan
  • Ismail Laher
  • Ayoub Saeidi
  • Urs Granacher
  • Hassane Zouhal

Objective: A role for microRNAs is implicated in several biological and pathological processes. We investigated the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on molecular markers of diabetic cardiomyopathy in rats. Methods: Eighteen male Wistar rats (260 ± 10 g; aged 8 weeks) with streptozotocin (STZ)-induced type 1 diabetes mellitus (55 mg/kg, IP) were randomly allocated to three groups: control, MICT, and HIIT. The two different training protocols were performed 5 days each week for 5 weeks. Cardiac performance (end-systolic and end-diastolic dimensions, ejection fraction), the expression of miR-206, HSP60, and markers of apoptosis (cleaved PARP and cytochrome C) were determined at the end of the exercise interventions. Results: Both exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, η2: 0.909). While the expressions of miR-206 and apoptotic markers decreased in both training protocols (p < 0.001, η2: 0.967), HIIT caused greater reductions in apoptotic markers and produced a 20% greater reduction in miR-206 compared with the MICT protocol (p < 0.001). Furthermore, both training protocols enhanced the expression of HSP60 (p < 0.001, η2: 0.976), with a nearly 50% greater increase in the HIIT group compared with MICT. Conclusions: Our results indicate that both exercise protocols, HIIT and MICT, have the potential to reduce diabetic cardiomyopathy by modifying the expression of miR-206 and its downstream targets of apoptosis. It seems however that HIIT is even more effective than MICT to modulate these molecular markers.

TidsskriftFrontiers in Cardiovascular Medicine
Antal sider11
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
The authors acknowledge the support of the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) – Project number 491466077 and Open Access Publishing Fund of the University of Potsdam, Germany. This work was financially supported by Alzahra University.

Publisher Copyright:
Copyright © 2022 Delfan, Amadeh Juybari, Gorgani-Firuzjaee, Høiriis Nielsen, Delfan, Laher, Saeidi, Granacher and Zouhal.

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