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The Response of Some Apoptotic Markers to Exercise Rehabilitation and Electrical Stimulation in Infarcted Rats

Year: 2024
Type: article
Abstract: Objectives: Apoptosis or scheduled death is an active and reversible biological process that plays a vital role in balancing cell growth and death in different tissues, particularly myocardial tissue in infarct patients. This research examined some of the apoptosis indices responses to an acute rehabilitation exercise (EX) and electrical stimulation (ES) in induced myocardial infarcted (MI) Wistar rats. Methods: In this experimental case-control study, 55 induced-MI Wistar rats (8 weeks old, mean weight: 220±30 g) were randomly assigned into 5 groups: Healthy, EX, exercise+ES, only ES and control group. The infarction was induced 24 hours after the subcutaneous injection of 150 mg/kg of isoproterenol. The EX and exercise plus ES groups performed a session of endurance exercise on an animal treadmill at 20 m/min for 1 hour. The ES was delivered by foot shock, set with an intensity of 0.2-0.5 mA for 20 minutes. Immediately after the cessation of the treatment protocol, cytochrome-C (Cyt-C), caspase-3 (CASP3), and CASP8 levels were measured by the ELISA method. Data analysis was performed using a 2-way analysis of variance (ANOVA) and the significance level was set at α=0.05. Results: Two-way ANOVA showed that the intervention in the infarction samples caused significant changes in the marker serum levels (P=0.0001). However, the procedure did not show significant changes in serum Cyt-C levels (P<0.05). Also, significant differences were observed in serum CASP8 concentrations between the MI, MI+EX+ES (P=0.02), MI+ES, and MI+EX+ES (P=0.02) groups. In addition, acute sports rehabilitation causes a significant decrease in CASP3 concentration among MI+EX and MI+EX+ES groups (P=0.01). Discussion: Exercise and ES decrease the serum levels of research CASP and reducing apoptosis favors the rehabilitation of MI samples.
Language: English
Field: Medicine
Open Access status: diamond
OpenAlex ID: W4404009051
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