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Mohammad Azimnezhad, Pezhman Motamedi, Mohammadreza Dehkhoda, Neda Khaledi,
Volume 20, Issue 23 (9-2022)
Abstract

Apoptosis is a programmed cell death and it’s associated with type 2 diabetes. The aim of present study was to investigate the effect of endurance training on caspase-3, Bcl-2 and Bax gene expression of cardiac tissue in type 2 diabetic male wistar rats.In an experimental trial, 36 male wistar rats were randomly divided into three groups, Diabetic Endurance Training (n=12), Diabetic Control (n=12) and Healthy Control (n=12). Type 2 diabetes was induced by intraperitoneal injection of STZ. The endurance training included 10 weeks, 5 sessions per week running at speed of 27 m/min for 20-30min in 1st week and reached to 27 m/min for 60 min/day in 10th weeks. The animals were sacrificed 24 h after last training session and the samples were taken from cardiac tissue. The gene expression of caspase-3, Bcl-2 and Bax were examined by Real time-PCR. The one-way ANOVA was used to analysis the data. The significant level was set at p<0.05. The gene expression of caspase-3and Bax of diabetic control group showed significant increase comparing with healthy control group (p =0.001) while gene expression of Bcl-2 significantly decreased (p =0.001). The endurance training induced significant reduction in the gene expression of caspase-3and Bax (p =0.001) and significant increase in the Bcl-2 compared to diabetic control group (p =0.001). It appears that gene expression of caspase-3, Bcl-2 and Bax of diabetic cardiac tissue are affected by positive effect of endurance training and the endurance training induces improvement in apoptosis of diabetic cardiac tissue.

Dr Majid Kashef, Dr Maral Ramez, Azam Ahmadi,
Volume 20, Issue 24 (3-2023)
Abstract

It is estimated that by 2035, more than 130 million adults will suffer from various types of cardiovascular diseases. Therefore, it is very important to know the pathogens of cardiac diseases and investigate new treatments. Also, despite continuous progress in diagnosis, patient education, and risk factor management, myocardial infarction (MI) remains one of the most common causes of morbidity, hospitalization, and mortality worldwide. The events associated with MI are highly complex and characterized by rapid metabolic and biochemical changes. Exercise training is an effective cardioprotective strategy that reduces adverse effects of MI and ischemia/reperfusion (I/R). Multiple signaling pathways of exercise preconditioning in mitigating MI-induced cardiac damage is one of the topics that has attracted much attention. In this article, some of the contributing factors in exercise-induced cardiac protection, including mitochondrial changes, metabolic changes, vascular adaptations, antioxidant capacity, heat shock proteins, cyclooxygenase levels, ATP-sensitive potassium channels, adenosine, protein kinase C, calcium and klotho homeostasis are discussed.
 


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