Volume 29, Issue 6 (9-2022)
RJMS 2022, 29(6): 144-154 |
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Research code: IR.IAU.K.REC.1400.092
Ethics code: IR.IAU.K.REC.1400.092
Clinical trials code: IR.IAU.M.R.EC1399.070
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Chenari M, Rahimi A, Sarshin A, Feizolahi F. Compare the Effect of Aerobic and Resistance Training on Bax and Caspase 3 Apoptotic Indices of the Heart Tissue in Male Diabetic Rats. RJMS 2022; 29 (6) :144-154
URL: http://rjms.iums.ac.ir/article-1-7210-en.html
URL: http://rjms.iums.ac.ir/article-1-7210-en.html
Department of Physical Education and Sport Science, Karaj Branch, Islamic Azad University, Karaj, Iran , a_r_rahimi@hotmail.com
Abstract: (773 Views)
Background & Aims: Diabetes is the most common metabolic disease in humans. It causes a group of metabolic disorders that are caused by decreased insulin secretion or resistance to its function. In general, diabetes mellitus refers to a heterogeneous group of metabolic disorders that is characterized by decreased insulin secretion, decreased insulin function, or both, and is divided into two main categories: type 1 diabetes and type 2 diabetes (1). Excessive blood sugar leads to irreversible damage to various parts of the body, especially the heart tissue. Damage to heart tissue in diabetics causes inflammation and destruction of heart cells, which in turn leads to apoptosis or cell death (2). Apoptosis or programmed cell death plays a key role in regulating the balance between reproduction and cell death in various tissues, especially somatic tissues such as the myocardium. It ends with the crumpling of the nucleus and cell membranes and the production of vacuoles containing apoptotic (3). Research has shown that BAX protein, by reducing the stability of the outer mitochondrial membrane, can lead to the release of apoptotic agents such as cytochrome C from the interstitial space. In the meantime, the common denominator of all apoptotic pathways is the activation of caspase-3 and the breakdown of vital cell proteins (4). Physical activity is one of the most effective ways to prevent diabetes and control it if you have the disease (8). Exercise is also known as one of the best non-pharmacological interventions in controlling apoptosis (9). Montazery taleghani et al. (2019) showed that eight weeks of resistance training led to a significant reduction in Bax gene expression and the ratio of bax to Bcl-2 in the heart tissue of diabetic rats (10). Arjmand et al. (2021) showed that endurance training significantly reduced the expression of caspase-3 and Bax genes in comparison with the diabetic control group (11). However, Kwak et al. (2006) reported that 12 weeks of exercise significantly increased left ventricular apoptosis (13). So far, no comprehensive study has been conducted, especially in the country, comparing the effect of aerobic and resistance training on cardiac muscle apoptosis during diabetes and possible molecular changes and proteins involved in apoptosis. It is expected that by conducting the present study, while answering some of the existing ambiguities and determining the effect of exercise on apoptosis, appropriate practical suggestions can be made on how to perform the exercise and also predict the possible consequences of aerobic and resistance training. Therefore, the aim of this study was to investigate compare the effect of aerobic and resistance training on Bax and Caspase 3 apoptotic indices of the heart tissue in male diabetic rats.
Methods: In this experimental study, 24 male Wistar rats were divided into six groups: aerobic training, resistance training, aerobic sham, resistance sham, control and healthy. Diabetes was induced by intraperitoneal injection of a single dose of streptozotocin. The aerobic and resistance training program was performed for six weeks. Western blotting was used to measure BAX and caspase-3. Data were analyzed by one-way analysis of variance and Tukey post hoc test at the P <0.05.
Results: The results showed that the mean difference of caspase-3 between aerobic training group with healthy and sham group (P=0.000), resistance training group with sham group (P=0.000) and aerobic training group with resistance training group (P=0.000), was significant and the amount of caspase-3 in the resistance training group was lower than aerobic training. There was a significant difference between the mean BAX between the aerobic training group with the healthy and sham groups (P=0.000), the resistance training group with the sham group (P=0.000) and the aerobic training group with the resistance training group (P=0.014). And BAX level in resistance training group was less than aerobic training.
Conclusion: The results of the present study showed that aerobic and resistance training led to a significant reduction in BAX levels in the heart tissue of diabetic rats and resistance training had a greater effect than aerobic exercise. The findings of this study were consistent with the results of Previous research (10,11,17). According to existing research, BAX protein plays an effective role in modulating cell death processes. Any factor that alters BAX levels leads the environment to apoptosis and inhibition of apoptosis (18,19). Normally, there is a balance between inhibitory factors and apoptotic stimuli, but in physiological and pathological situations, this balance is always disturbed, and one of these situations is physical activity. It is possible that exercise activities can prevent cell death by affecting the most important factors affecting the apoptotic process (20). Regular exercise increases myocardial BCl2 protein and changes the ratio of BAX to BCl2 to an anti-apoptotic medium (21). Activation of the BAX protein increases the permeability of the mitochondrial membrane. One of the important biological aspects of mitochondria is the role that this organ plays in apoptosis. Mitochondria are an integral part of the internal pathway of apoptosis and the locus of many proteins involved in the early stages of this process, including members of the BCl2 family (22). BAX entry into mitochondria and release of cytochrome C triggers apoptotic signaling of downstream caspase cascades (21). Evidence suggests that regular exercise (resistance and endurance) can counteract the (onset of cardiovascular disease) apoptosis of diabetic rat heart cells and its adverse consequences. Also, the results of our study showed that aerobic exercise has a significant effect on reducing the amount of caspase-3 in the heart tissue of diabetic rats. On the other hand, resistance training has a significant effect on reducing the amount of caspase-3 in the heart tissue of diabetic rats. This finding is consistent with the findings of some previous studies that have reported a decrease in caspase-3 after exercise (24-27). Caspase-3 is activated by activating caspase-12 through the calcium release pathway or by activating caspase-9 internally or by increasing serum TNF-α externally (21). The exact mechanisms of exercise-induced apoptosis are unclear. Mitochondria and endoplasmic reticulum in the internal pathway are the focus of the process, in which the focus of mitochondria has been the most important in causing apoptosis (1). Under stress, factors such as glucocorticoids, ROS, nitrogen monoxide, chemotherapy drugs, radiation, reduced growth stimulants, and cytokines cause changes in mitochondrial stress, causing changes in its permeability, and cytochrome c in the inner membrane and cytokine. It is located between the membranes, is released into the cytosol, binds to apoptosis-activating factor 1 protease 1, and forms a compound called dATP. This compound then induces apoptosis by activating procaspase 9, caspase 9, and caspase 3 (32). Inhibitors of cell death pathway proteins such as Bcl- 2 and Bcl-XL inhibit the release of cytochrome c and thus play a role (33). According to the results of studies, it can be said that regular resistance and endurance activity of each separately in the present study, is an effective factor in reducing the expression of caspase-3 in preventing cardiac cell apoptosis in male Wistar diabetic rats. One of the limitations of the present study is the lack of measurement of other apoptotic markers in cardiac tissue. It is also suggested that BCL-2 anti-apoptotic factor and inflammatory markers for their relationship with apoptotic markers in cardiac tissue of diabetic specimens for better explanation and interpretation. Measure the results. According to the findings of the present study, exercise can reduce the effects of diabetes on cardiac cell apoptosis in male Wistar rats. It is on the control of apoptotic signaling pathway in diabetic rats. Therefore, the use of both resistance and aerobic exercise is recommended as effective treatments to reduce the apoptosis of heart cells in male Wistar diabetic rats. Meanwhile, the effect of resistance training on reducing the complications of diabetes on cardiac tissue apoptotic factors was greater than aerobic exercise and closer to the levels of pre-apoptotic factors in the healthy group.
Methods: In this experimental study, 24 male Wistar rats were divided into six groups: aerobic training, resistance training, aerobic sham, resistance sham, control and healthy. Diabetes was induced by intraperitoneal injection of a single dose of streptozotocin. The aerobic and resistance training program was performed for six weeks. Western blotting was used to measure BAX and caspase-3. Data were analyzed by one-way analysis of variance and Tukey post hoc test at the P <0.05.
Results: The results showed that the mean difference of caspase-3 between aerobic training group with healthy and sham group (P=0.000), resistance training group with sham group (P=0.000) and aerobic training group with resistance training group (P=0.000), was significant and the amount of caspase-3 in the resistance training group was lower than aerobic training. There was a significant difference between the mean BAX between the aerobic training group with the healthy and sham groups (P=0.000), the resistance training group with the sham group (P=0.000) and the aerobic training group with the resistance training group (P=0.014). And BAX level in resistance training group was less than aerobic training.
Conclusion: The results of the present study showed that aerobic and resistance training led to a significant reduction in BAX levels in the heart tissue of diabetic rats and resistance training had a greater effect than aerobic exercise. The findings of this study were consistent with the results of Previous research (10,11,17). According to existing research, BAX protein plays an effective role in modulating cell death processes. Any factor that alters BAX levels leads the environment to apoptosis and inhibition of apoptosis (18,19). Normally, there is a balance between inhibitory factors and apoptotic stimuli, but in physiological and pathological situations, this balance is always disturbed, and one of these situations is physical activity. It is possible that exercise activities can prevent cell death by affecting the most important factors affecting the apoptotic process (20). Regular exercise increases myocardial BCl2 protein and changes the ratio of BAX to BCl2 to an anti-apoptotic medium (21). Activation of the BAX protein increases the permeability of the mitochondrial membrane. One of the important biological aspects of mitochondria is the role that this organ plays in apoptosis. Mitochondria are an integral part of the internal pathway of apoptosis and the locus of many proteins involved in the early stages of this process, including members of the BCl2 family (22). BAX entry into mitochondria and release of cytochrome C triggers apoptotic signaling of downstream caspase cascades (21). Evidence suggests that regular exercise (resistance and endurance) can counteract the (onset of cardiovascular disease) apoptosis of diabetic rat heart cells and its adverse consequences. Also, the results of our study showed that aerobic exercise has a significant effect on reducing the amount of caspase-3 in the heart tissue of diabetic rats. On the other hand, resistance training has a significant effect on reducing the amount of caspase-3 in the heart tissue of diabetic rats. This finding is consistent with the findings of some previous studies that have reported a decrease in caspase-3 after exercise (24-27). Caspase-3 is activated by activating caspase-12 through the calcium release pathway or by activating caspase-9 internally or by increasing serum TNF-α externally (21). The exact mechanisms of exercise-induced apoptosis are unclear. Mitochondria and endoplasmic reticulum in the internal pathway are the focus of the process, in which the focus of mitochondria has been the most important in causing apoptosis (1). Under stress, factors such as glucocorticoids, ROS, nitrogen monoxide, chemotherapy drugs, radiation, reduced growth stimulants, and cytokines cause changes in mitochondrial stress, causing changes in its permeability, and cytochrome c in the inner membrane and cytokine. It is located between the membranes, is released into the cytosol, binds to apoptosis-activating factor 1 protease 1, and forms a compound called dATP. This compound then induces apoptosis by activating procaspase 9, caspase 9, and caspase 3 (32). Inhibitors of cell death pathway proteins such as Bcl- 2 and Bcl-XL inhibit the release of cytochrome c and thus play a role (33). According to the results of studies, it can be said that regular resistance and endurance activity of each separately in the present study, is an effective factor in reducing the expression of caspase-3 in preventing cardiac cell apoptosis in male Wistar diabetic rats. One of the limitations of the present study is the lack of measurement of other apoptotic markers in cardiac tissue. It is also suggested that BCL-2 anti-apoptotic factor and inflammatory markers for their relationship with apoptotic markers in cardiac tissue of diabetic specimens for better explanation and interpretation. Measure the results. According to the findings of the present study, exercise can reduce the effects of diabetes on cardiac cell apoptosis in male Wistar rats. It is on the control of apoptotic signaling pathway in diabetic rats. Therefore, the use of both resistance and aerobic exercise is recommended as effective treatments to reduce the apoptosis of heart cells in male Wistar diabetic rats. Meanwhile, the effect of resistance training on reducing the complications of diabetes on cardiac tissue apoptotic factors was greater than aerobic exercise and closer to the levels of pre-apoptotic factors in the healthy group.
Type of Study: Research |
Subject:
Exercise Physiology
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