|
Skeletal muscle as the spokesman for the movement of the human body, in order to create and maintain mechanical tension, the muscle cells show highly structured organization. Muscle cells all the time in the event of changes, including some changes in the decomposition conditions: protein is mobilized, mitochondria and sarcoplasmic reticulum remodeling, such as muscle cell nuclei disappeared. Daily physical activity, muscle contraction can cause damage to the mechanical and metabolic muscle proteins and organelles, or a change. It has been in the aging process the catabolism to strengthen the body from a series of changes need to strengthen the the autophagy pathway dysfunction and the abolition of the molecular Clear, autophagy related genes have a close relationship with skeletal muscle aging process. Physical exercise can promote the body metabolism, effectively delaying cell aging, reduce the probability of cancerous cells, this process may have a benign effect on autophagy. The tumor suppressor protein p53 \However, skeletal muscle autophagy, especially mitochondrial autophagy pathway gene expression mechanisms specific exercise specifically since the little-known, and little is known about the motion sensitive gene expression regulatory factors. Objective: To observe the four-week endurance exercise and p53 inhibitor 40-week-old ICR mouse skeletal muscle autophagy gene expression, transcription the of ICR mice p53/ARF and PUMA / BAX signaling pathway gene expression of autophagy mitochondria from the role of the body phagocytic and oxidative function control to a new understanding of the mitochondrial theory of aging, and new explorations through their impact exercise intervention. Methods: 40 male ICR, 40 weeks old, weighing 45 ± 5g were randomly divided into control group, n = 8 of Pifithrin-α groups, Pifithrin-α endurance training group, Pifithrin-μ group, Pifithrin-μ endurance training. The Endurance Training Pifithrin-α and Pifithrin-μ endurance training four weeks of treadmill training, training six days a week, once a day, training 40 minutes. After feeding, the end of the last movement of the rats in each group were executed in 12-24h, compare with the microplate reader measured the activity of T-SOD, GSH concentration; Real-time PCR determination of the rat gastrocnemius p53 mRNA, Bax mRNA Beclin-1 mRNA LC3 mRNA and Atg7mRNA levels for comparison. Results: (1) Experiment 4 weeks after the P-α group, P-α Training Unit, P-μ group, P-μ training group compared with the C group, there was no significant difference; comparison of P-α Training and Pa, P-μ training group compared with the P-μ group, also showed no significant differences. (2) antioxidant capacity: SS mitochondrial P-α group and C group comparison GSH was extremely significant with upregulation; IMF mitochondria, P-α training group of GSH and C group comparison significant with upregulation; P-α group T-SOD activity significantly raised, Pa training group T-SOD activity was significantly raised compared Pa group compared with C group. (3) P-α training group and P-μ training group and C group compare P53 mRNA in significantly with raised; P-μ group P-α training group and the P-μ training group and C group comparison Beclin-1 mRNA extremely significant with raised , P-α training group with P-α group comparison, P-μ group with P-μ training group comparison Beclin-1 mRNA extremely significant with upregulation; P-μ group, P-α training group and P-μ training group with Bax mRNA in group C was significantly raised P-μ group was highly significant upregulation of Beclin-1 mRNA compared training group P-μ. (4) P-μ training group and group C compare of LC3 mRNA and Atg7mRNA of extremely significant upregulation; of LC3 mRNA endurance exercise group P of P-μ-μ training group and Atg7mRNA very significant upward. Conclusion: (1) endurance training and the p53 inhibitor did not affect the weight of aging ICR mice (2) in the mitochondrial subfractions, increasing age and injection of p53 inhibitor induced oxidative stress injury and whether endurance exercise have been alleviated the effect is different. (3) endurance training can upregulate autophagy genes LC3, Atg7, Beclin-1 mRNA that autophagy enhanced trend, may need to clear more functional defect molecule catabolism during exercise to strengthen. (4) p53 inhibitor p53 pathway on mitochondrial autophagy may impact autophagy related gene transcription by.
|