| Objective: A rat gastrocnemius contusion experimental model was made. The fusion-fission gene expression of rats were observed after contusion to explore the mitochondrial fission and fusion gene expression in the rat gastrocnemius contusion repair process, clarify the mitochondrial quality control mechanism in autologous repair after the gastrocnemius is injuried, provide the theoretical basis for exploring gastrocnemius injury repair limiting factors from the perspective of energy metabolism in the next step, and to be of great significance in studying exogenous control injury repair speed.Method: The 60 male Wistar rats were randomly divided into 8 groups named as 12 h group, 2D group, 5D group, 7d group, 10 d group, 15 d group, 30 d group and control group. After hitting the gastrocnemius of the two hind legs of the Wistar rats in the former seven groups by using a self-made contusion hitter, the former seven groups are sequentially sampled immediately 12 hours, 2 days, 5 days, 7 days, 10 days, 15 days and 30 days after contusion hitting. While the control group and 12 h group were sampled on the same day, and RNA was extracted from the gastrocnemius of the two hind legs of the Wister rats. The total RNA was taken as a template. Transcription was reversed into c DNA by reverse transcriptase. c DNA was taken as the template for PCR amplification, thus the expression of the rat mitochondrial fusion-fission gene was obtained.Result: 1.the expression, mitochondrial fusion gene splitting, look for the overall performance from the change trend of 12 h, 2D, 5D, 7d, 10 d, 15 d, 30 d were significantly decreased gradually: compared with the normal control group, the total amount of each expression showed a rising trend, the general trend in the expression of 2D, 10 d in two stages volume decline, 2D gene expression level to the lowest value, 15 d, 30 d gene expression at the maximum value.2. The expression quantity of mitochondrial fusion genes of the 30 d group was lower than that of normal control group, DPR1 gene of mitochondrial fission of the 30 d group was higher than that of the normal control group, Fist1 of the 30 d group was lower than that of normal control group.3.Changes of mitochondrial fusion gene in 12 h group, 2d group, 5d group and 10 d group were quite obvious compared with the control group, were significantly decreased. Mitochondrial fission gene only changed quite significantly in the 2d group.Conclusions:(1) expression of mitochondrial fusion fission gene reached the lowest value at 2D, in the inflammatory reaction stage, mitochondrial respiratory inhibition, decreased function of fusion-fission function, fusion gene resulted in a decrease in energy supply shortages, slow recovery rate. The expression of 10 d decreased mechanism is not clear.(2) consistent with mitochondrial fusion-fission gene expression on the expression amount of the overall trend, but slightly higher than the mitochondrial fission gene expression of fusion gene, and re allocation of mitochondrial fission and gene regulation of cell apoptosis and energy. Mitochondrial tends to split may be caused by the decrease in mitochondrial respiratory function, and reduce the increase of fusion, splitting is helpful to improve the metabolic efficiency, provide enough energy for a new cell.(3) expression in the 30 day of mitochondrial fusion gene splitting tend to normal levels but overall is still lower than normal, in the repair period of fibrous tissue and muscle tissue hyperplasia at birth at the same time, the poor level of mitochondrial fusion energy supply is insufficient, make the site of injury recovery is not complete, mitochondrial dynamic balance body fusion division did not reach the best the level of. Mitochondrial fusion- a highly dynamic balance of cell division actively and effectively adapt to the new environment plays an important role, is conducive to the recovery after injury. |
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