The effect of a period of aerobic endurance training before isoproterenol induction on the expression of NF-κB and NFAT genes in the left ventricular tissue of male Wistar rats

Document Type : original article

Authors

1 Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran

2 .Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran

Abstract

Background and Purpose: Pathogenic cardiac hypertrophy is a type of heart disorder that is associated with changes in the structure of the heart, apoptosis and fibrosis of the heart muscle cells, which leads to a decrease in the pumping ability of the heart and may eventually lead to heart failure and sudden death. It has been shown that the signaling pathway of transcription factors NF-κB and NFAT play an important role in the process of pathogenic hypertrophy of the heart, and considering that few studies have investigated the effect of exercise on these factors in the process of pathogenic hypertrophy,the aim of the present study was to identify the effect of eight weeks of aerobic exercise before isoproterenol induction on the expression of NF-κB and NFAT genes in the left ventricular tissue of male Wistar rats.
Materials and Methods: 18 male Wistar rats were randomly divided into two groups of endurance training and control. Endurance training was performed for eight weeks, one hour a day and six days a week on a treadmill with a slope of 15 degrees. After eight weeks of training, pathological hypertrophy was induced by subcutaneous injection of three mg / kg isoprenaline for seven days. 24 hours after the last injection session, rats were anesthetized by intraperitoneal injection of 50 mg ketamine and 10 mg xylazine. The rats were then dissected and cardiac tissue was extracted and transferred to -70 ° C. Also, in the present study, Real Time PCR was used to evaluate the expression of NF-κB and NFAT genes. Data analysis was performed using SPSS software version 24 and independent t-test at a significance level of P ≥ 0.05
Results: The results of the present study showed that the indices of heart weight, heart weight to body weight ratio (H / W) and left ventricular weight to body weight ratio (V / W) were significantly (P = 0.01) and (P = 0.03): Respectively, increased in the exercise group compared to the control group. Also, the relative expression of NF-κB gene was significantly (P = 0.03) decreased in the exercise group compared to the control group, while the relative expression of NFAT gene was not significantly changed in the study groups (P = 0.40).
Conclusion: Eight weeks of aerobic endurance training may play an important role in the prevention of pathological cardiac hypertrophy by reducing the relative expression of the NF-κB gene.

Keywords

References

  1. Siddiqui M, Ahmad U, Khan A, Ahmad M, Badruddeen KM, Akhtar J. Isoprenaline: a tool for inducing myocardial infarction in experimental animals. Int J Pharm. 2016;6(2):138-44.
  2. Hall J. Guyton and Hall textbook of medical physiology e-Book: Elsevier Health Sciences. 2015.
  3. Tham YK, Bernardo BC, Ooi JY, Weeks KL, McMullen JR. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Archives of toxicology. 2015;89(9):1401-38.
  4. Chen Y, Pan R, Zhang J, Liang T, Guo J, Sun T, et al. Pinoresinol diglucoside (PDG) attenuates cardiac hypertrophy via AKT/mTOR/NF-κB signaling in pressure overload-induced rats. Journal of Ethnopharmacology. 2021;272:113920.
  5. Shimizu I, Minamino T. Physiological and pathological cardiac hypertrophy. Journal of molecular and cellular cardiology. 2016;97:245-62.
  6. Yu X-J, Zhang D-M, Jia L-L, Qi J, Song X-A, Tan H, et al. Inhibition of NF-κB activity in the hypothalamic paraventricular nucleus attenuates hypertension and cardiac hypertrophy by modulating cytokines and attenuating oxidative stress. Toxicology and Applied Pharmacology. 2015;284(3):315-22.
  7. Ma D, Zhang J, Zhang Y, Zhang X, Han X, Song T, et al. Inhibition of myocardial hypertrophy by magnesium isoglycyrrhizinate through the TLR4/NF-κB signaling pathway in mice. International immunopharmacology. 2018;55:237-44.
  8. Yin Z, Wang X, Zhang L, Zhou H, Wei L, Dong X. Aspirin Attenuates Angiotensin II‐induced Cardiomyocyte Hypertrophy by Inhibiting the Ca2+/Calcineurin‐NFAT Signaling Pathway. Cardiovascular therapeutics. 2016;34(1):21-9.
  9. Wackerhage H. Molecular exercise physiology: an introduction: Routledge; 2014.
  10. Liu Q, Chen Y, Auger-Messier M, Molkentin JD. Interaction between NFκB and NFAT coordinates cardiac hypertrophy and pathological remodeling. Circulation research. 2012;110(8):1077-86.
  11. Fiuza-Luces C, Santos-Lozano A, Joyner M, Carrera-Bastos P, Picazo O, Zugaza JL, et al. Exercise benefits in cardiovascular disease: beyond attenuation of traditional risk factors. Nature Reviews Cardiology. 2018;15(12):731-43.
  12. Lear SA, Hu W, Rangarajan S, Gasevic D, Leong D, Iqbal R, et al. The effect of physical activity on mortality and cardiovascular disease in 130 000 people from 17 high-income, middle-income, and low-income countries: the PURE study. The Lancet. 2017;390(10113):2643-54.
  13. Barzegari Marvast H, Choobineh S, Soori R, Akbarnejad A. The Effect of 16 weeks of intense endurance training on right ventricle structure in male Wistar rats. Journal of Sport and Exercise Physiology. 2021;14(1):95-107.(In Persian).
  14. Pandey A, LaMonte M, Klein L, Ayers C, Psaty BM, Eaton CB, et al. Relationship between physical activity, body mass index, and risk of heart failure. Journal of the American College of Cardiology. 2017;69(9):1129-42.
  15. Hering D, Lachowska K, Schlaich M. Role of the sympathetic nervous system in stress-mediated cardiovascular disease. Current hypertension reports. 2015;17(10):1-9.
  16. Ren J, Yang L, Tian W, Zhu M, Liu J, Lu P, et al. Nitric oxide synthase inhibition abolishes exercise-mediated protection against isoproterenol-induced cardiac hypertrophy in female mice. Cardiology. 2015;130(3):175-84.
  17. Tabrizi A, Soori R, Choobineh S, Gholipour M. Role of Endurance Training in Preventing Pathological Hypertrophy via Large Tumor Suppressor (LATS) Changes. Iranian Heart Journal. 2019;20(3):52-9.
  18. Wisløff U, Helgerud J, Kemi OJ, Ellingsen Ø. Intensity-controlled treadmill running in rats: V̇ o 2 max and cardiac hypertrophy. American journal of physiology-heart and circulatory physiology. 2001;280(3):H1301-H10.
  19. Kemi OJ, Haram PM, Loennechen JP, Osnes J-B, Skomedal T, Wisløff U, et al. Moderate vs. high exercise intensity: differential effects on aerobic fitness, cardiomyocyte contractility, and endothelial function. Cardiovascular research. 2005;67(1):161-72.
  20. Zhou L, Ma B, Han X. The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy. Journal of Molecular Endocrinology. 2016;57(4):R143-R52.
  21. Gaeini A, Kazemi F, Mehdiabadi J. Comparing the effect of aerobic continuous and interval training and detraining on cardiac hypertrophy and atrophy. J Physiol Exer Physic Act. 2010;3(2):499-506.
  22. Smith DL, Fernhall B. Advanced cardiovascular exercise physiology: Human Kinetics; 2011.
  23. Yang M, Lim CC, Liao R, Zhang X. A novel microfluidic impedance assay for monitoring endothelin-induced cardiomyocyte hypertrophy. Biosensors and Bioelectronics. 2007;22(8):1688-93.
  24. Ma D, Zhang J, Zhang Y, Zhang X, Han X, Song T, et al. Inhibition of myocardial hypertrophy by magnesium isoglycyrrhizinate through the TLR4/NF-κB signaling pathway in mice. International immunopharmacology. 2017;55:237-44.
  25. Xu T, Tang H, Zhang B, Cai C, Liu X, Han Q, et al. Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy. International journal of clinical and experimental pathology. 2015;8(1):530.
  26. Serra AJ, Santos MH, Bocalini DS, Antônio EL, Levy RF, Santos AA, et al. Exercise training inhibits inflammatory cytokines and more than prevents myocardial dysfunction in rats with sustained β‐adrenergic hyperactivity. The Journal of physiology. 2010;588(13):2431-42.
  27. Farrell PA, Joyner MJ, Caiozzo V. ACSM's advanced exercise physiology: Wolters Kluwer Health Adis (ESP); 2011.
  28. Baghaiee B, Bayatmakoo R, Karimi P, Pescatello LS. Moderate Aerobic Training Inhibits Middle-Aged Induced Cardiac Calcineurin-NFAT Signaling by Improving TGF-ß, NPR-A, SERCA2, and TRPC6 in Wistar Rats. Cell Journal (Yakhteh). 2021;23(7):756.
  29. Oliveira R, Ferreira J, Gomes E, Paixao N, Rolim NPL, Medeiros A, et al. Cardiac anti‐remodelling effect of aerobic training is associated with a reduction in the calcineurin/NFAT signalling pathway in heart failure mice. The Journal of physiology. 2009;587(15):3899-910.
  30. Oliveira R, Ferreira J, Gomes E, Paixao N, Rolim N, Medeiros A, et al. Cardiac anti‐remodelling effect of aerobic training is associated with a reduction in the calcineurin/NFAT signalling pathway in heart failure mice. The Journal of physiology. 2009;587(15):3899-910.
  31. McMorris T. Developing the catecholamines hypothesis for the acute exercise-cognition interaction in humans: Lessons from animal studies. Physiology & behavior. 2016;165:291-9.
  32. Marom M, Birnbaumer L, Atlas D. Membrane depolarization combined with Gq-activated G-protein-coupled receptors induce transient receptor potential channel 1 (TRPC1)-dependent potentiation of catecholamine release. Neuroscience. 2011;189:132-45.

33.          Seth M, Zhang Z-S, Mao L, Graham V, Burch J, Stiber J, et al. TRPC1 channels are critical for hypertrophic 

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History

  • Receive Date: 05 June 2022
  • Revise Date: 01 August 2022
  • Accept Date: 09 August 2022
  • First Publish Date: 23 August 2022
  • Publish Date: 23 August 2022

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