مجله دانشکده پزشکی اصفهان (Aug 2019)

The Interactive Effect of Forced Swimming and Crocin Supplementation on the Expression of BAX and BCL-2 Cardiomyocyte Genes in Male Rats Infected with Hydrogen Peroxide

  • Mina Akbari,
  • Fereshteh Shahidi,
  • Hamid Rajabi,
  • Majid Kashef,
  • Zohreh Mazaheri

DOI
https://doi.org/10.22122/jims.v37i525.11085
Journal volume & issue
Vol. 37, no. 525
pp. 443 – 453

Abstract

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Background: The aim of this study was to determine the interaction effect of forced swimming and crocin supplementation on the expression of BAX and BCL-2 cardiomyocyte genes in male rats poisoned by hydrogen peroxide (H2O2). Methods: 36 male Wistar rats were randomly divided into six groups of sham, H2O2, H2O2 and crocin, H2O2 and forced swimming, H2O2 and crocin and forced swimming, and control. The forced swimming protocol was 60 minutes, 5 days a week, for 6 weeks. H2O2 (1 mg/kg for 3 weeks) and crocin (12.5 Mm/kg daily with 5 cc of distilled water) were injected intraperitoneally. Real time polymerase chain reaction (PCR) device was used to assess gene expression, and apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Statistical analysis was done using Kolmogorov-Smirnov, Levene, one-way ANOVA and, the Scheffe post hoc tests. Findings: H2O2 induction was associated with a significant increase in the apoptosis of BAX (P < 0.001). Six weeks of exercise in water tended to reduction in the BCL-2 expression (P = 0.023), and induction of crocin resulted in significant decrease in BAX expression. The interaction between swimming, crocin and H2O2 decreased BAX and increased BCL-2 expression, which indicated the protective effect of regular activity in reducing cardiomyocyte apoptosis. Conclusion: Forced swimming as well as the use of crocin separately led to a significant reduction in BAX gene expression and a significant increase in BCL-2 gene expression. On the other hand, the combination of exercise and crocin had synergistic and synergistic effects in inhibiting the apoptotic expression of BAX and also enhancing the expression of the anti-apoptotic gene of BCL-2 in rats poisoned by H2O2.

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