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Endurance training and MitoQ supplementation increase PERM1 and SMYD1 gene expression and improve hemodynamic function in cardiac muscle of male Wistar rats

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  • معلومة اضافية
    • بيانات النشر:
      Kerman University of Medical Sciences, 2024.
    • الموضوع:
      2024
    • Collection:
      LCC:Immunologic diseases. Allergy
      LCC:Diseases of the circulatory (Cardiovascular) system
    • نبذة مختصرة :
      Background:The histone methyltransferase (SMYD1) and the muscle-specific protein (PERM1) play an important role in maintaining cardiac energetics and function. The present study aimed to examine the effect of two types of endurance training (running and swimming) plus MitoQ supplementation on gene expression of PERM1 and SMYD1 plus hemodynamic function in the cardiac muscle of male Wistar rats.Methods: The animals underwent MitoQ supplementation or endurance training or endurance training + MitoQ supplementation for eight weeks. Gene expression of PERM1 and SMYD1, measured by Real Time-PCR and quantified by 2-∆∆CT method, and hemodynamic function were compared between groups using two-way multivariate analysis of variance. Results: Cardiac gene expression of PERM1 and SMYD1 increased significantly through running (PERM1, P < 0.05; SMYD1, P < 0.01), swimming (PERM1, P < 0.05; SMYD1, P < 0.05). and MitoQ supplementation (PERM1, P < 0.001). The effects of MitoQ supplementation were additive to both running and swimming effects on cardiac gene expression of (PERM1, P < 0.001; SMYD1, P < 0.05). Swimming-induced enhancement in cardiac expression of PERM1 and SMYD1 was associated with a significant increase in ±dP/dt max (P < 0.05)). Conclusion: Expression of genes involved in cardiac metabolism can be affected by endurance training and this effect could be improved through MitoQ supplementation
    • File Description:
      electronic resource
    • ISSN:
      1023-9510
      2008-2843
    • Relation:
      https://jkmu.kmu.ac.ir/article_92273_bf45c9a1c70e3b355e33ba5f6d551163.pdf; https://doaj.org/toc/1023-9510; https://doaj.org/toc/2008-2843
    • الرقم المعرف:
      10.34172/jkmu.2023.53
    • الرقم المعرف:
      edsdoj.544d739fa242e99de4fb6e60b2ed9e