[Animal Experiment]-The regulatory mechanism of protein conversion in skeletal muscle atrophy induced by hypoxia exposure

  OBJECTIVE: To compare the differences between hypoxic exposure and hypoxic feeding intervention (semi-starvation) combined with hypoxic exposure on the expression of genes related to protein synthesis and degradation in rat skeletal muscle. Explore the possible mechanism of skeletal muscle atrophy?

  Methods: SD rats were divided into the following categories: (1) Normal oxygen intake group (Group C); (2) Normal oxygen intake group (Group H), with an oxygen concentration of 12.4%; (3) Normal intake group The food intake of the oxygen and diet group (P group), that is, the food intake of group H the day before? After 4 weeks of intervention, measure the body composition of the rat, measure the flat head muscle (SOL) and extensor digitorum longus (EDL), measure the wet weight; observe the shape of muscle fibers by HE staining, and calculate the cross-sectional area of muscle fibers (FCSA); WB Test the protein content of HIF1α? Akt? Genes related to p-Akt and skeletal muscle protein synthesis and degradation in skeletal muscle?

  Results: 1) There was no significant difference in the body weight of the rats in the H group. Compared with the C group, the P group and the C group, the two groups continued to decline. At the beginning of the intervention, the food intake of group H (same as group P) was significantly lower than that of group C, and there was no difference between the two groups in later periods. (2) After the intervention, the body weight and total muscle mass of rats in group H were higher than those in group C. The P group was significantly reduced, and there was no difference between the P and C groups; the wet weight of the two muscles in the H group was significantly lower than that of the C group; the FCSA of the HDL EDL was C. and was significantly lower than the P group; (3) H group The protein content of HIF1α in EDL was significantly higher than that in group C; the ratio of p-Akt/Akt in SOL of H and P groups was significantly lower than that of group C; the protein content of mTOR 4EBP1 in EDL of H group was significantly lower than that of Atrodin1α in C group. MuRF1? The protein content of Beclin 1 and the ratio of LC3II/I were significantly higher than that of group C. The MuRF1 protein content of SOL in group H was significantly higher than that of group C and P? Group ratio.

  Conclusion: The skeletal muscle atrophy caused by hypoxia is caused by hypoxia-specific factors and manifests as fast muscle. Isn't the decrease in skeletal muscle protein synthesis and increase in degradation caused by reduced food intake under hypoxic conditions?