| Skeletal muscle movement as the spokesman for the body, in order to create and maintain the mechanical tension, muscle cells are highly structured organization. Muscle cells are in the event of various changes all the time, including some of the changes in the decomposition conditions:the protein mobilizing, mitochondria and sarcoplasmic reticulum remodeling, muscle cell nucleus disappearing. Daily physical activity and muscle contraction can lead to mechanical and metabolic muscle protein and organelle damage or change. Studies suggest that in the aging process catabolism is strengthened, a series of body changes need to strengthen the autophagy pathway for theb functional impairment and the abolition of molecules removed. Autophagy-related genes are closely related to the aging process in skeletal muscle. Physical exercise can promote the body's metabolism, effectively delay the cell aging and reduce the chances of cancerous cells, so we consider that the process of autophagy may have a positive effect. Tumor suppressor protein "genes Guardian" p53, involved in the regulation of autophagy is a cellular energy metabolism, oxidative stress signals to maintain cell homeostasis, prevention of cancer and anti-aging strategies. However, autophagy in skeletal muscle, especially in the way of mitochondrial movement of specific autophagy pathway-specific gene expression mechanism is still unknown, the sensitivity of gene expression and exercise of regulatory factors is also poorly understood.Objective:To observe the effect of 4-week endurance exercise, and p53 inhibitor on the 40-week-old ICR mouse skeletal muscle autophagy-related gene expression, through the effects of ICR mice p53/ARF and PUMA/BAX pathway related gene expression and transcription of autophagy, mitochondrial autophagy and the role of oxidative control to study the impact of aging on mitochondrial theory, and observe the impact of the exercise intervention.Methods:40 male ICR mice(40 weeks old, weight 45±5g) were randomly divided into control group, Pifithrin-αgroup, Pifithrin-αendurance training group, Pifithrin-μ group, Pifithrin-μendurance training group, each group has 8. Pifithrin-a endurance training group and Pifithrin-μendurance training group have 4 weeks treadmill training(6 days a week, once a day, training for 40 minutes). After the last time of the exercise within 12-24h the rats were sacrificed, measured the concentration of GSH and the activity of T-SOD with a microplate reader to compared with each group, and measured the rat gastrocnemius p53 mRNA, Bax mRNA, Beclin-1 mRNA, LC3 mRNA levels and Atg7mRNA with Real-time PCR.Results:(1)4 weeks experiment later, P-αgroup, P-a training group, P-μgroup, P-μtraining group were compared with C group, there was no significant difference; P-αtraining group compared with P-αgroup, P-μtraining group compared with the P-μ,were also no significant difference.(2) Antioxidant capacity:In SS mitochondria, the GSH concentration of P-αgroup compared with C group was significant increase; In IMF mitochondria, the GSH concentration of P-αTraining group compared with C group significantly increased; the T-SOD activity of P-αgroup Compared with C group was significantly increased; the T-SOD activity of P-αtraining group compared with P-αgroup was significantly increased.(3) P-αtraining group and P-μtraining group compared with C group p53 mRNA was significantly upregulated; P-μgroup, P-αtraining group and P-μtraining group compared with C group Beclin-1 mRNA was significantly increased, P-αtraining group compared with P-αgroup, P-μgroup compared with P-μtraining group Beclin-1 mRNA was significant increased; P-μgroup, P-αtraining group and P-μtraining group compared with C group Bax mRNA was significantly increased, P-μgroup compared with P-μtraining group Beclin-1 mRNA was significant increased.(4) P-μtraining group compared with C group Atg7mRNA and LC3 mRNA were significant increased; P-μendurance exercises group compared with P-μgroup LC3 mRNA and Atg7mRNA were significant increase.Conclusion: (1) Endurance training and the p53 inhibitor had no effect on body weight of mice aged ICR(2)In the mitochondrial sub-fractions, and the injection of p53 inhibitor of aging caused by oxidative stress injury and can be mitigated by the effect of endurance exercise are different.(3)Endurance training can increase autophagy-related genes LC3, Atg7, Beclin-1mRNA.The results show that autophagy can enhance the trend of increasing catabolism during exercise, and more features need to clear the molecular defect.(4) The inhibitors of p53 on mitochondria may influence autophagy pathway related gene transcription by autophagy.
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