| Background : Aging is a natural life phenomenon.Health and longevity is the eternal theme of medical research.How to delay aging is a hot issue in society and academic circles.With the increase of age,skeletal muscle appears the phenomenon of decreased muscle mass,strength and physical activity,the ubiquitin proteasome pathway induces increased skeletal muscle protein breakdown,which is called skeletal muscle attenuation.It has been found that resistance training can delay skeletal muscle attenuation,but its biological mechanism needs to be further clarified.Skeletal muscle satellite cells are stem cells in muscle tissue,which are closely related to the growth,development and repair and remodeling of skeletal muscle.Resistance training can activate and proliferate skeletal muscle satellite cells,suggesting that skeletal muscle satellite cell cycle is triggered and then mitosis occurs.Whether the mechanism of resistance training to delay skeletal muscle aging plays a role in cyclin in skeletal muscle satellite cells needs further study.Objective : Exercise intervention was carried out in C57BL/6J aging mice by anti-impedance training.The purpose of this study was to explore the effect of anti-impedance training on skeletal muscle satellite cells and their cyclin.To provide theoretical basis for anti-impedance training to delay skeletal muscle senescence.Methods:C57BL/6J strain mice were studied in this study,16 2-month-old mice,Feed to 18 months old in IVC independent air supply system,To establish a natural aging mouse model.The mice aged 18 months were randomly divided into two groups: quiet control group(C group: n=8),Free diet,drinking water,Do not participate in sports training.Resistance training group(R group: n=8)carries out resistance training for 8 weeks every Monday,Wednesday and Friday in the form of tail load climbing ladder.Every Monday,the maximum weight was measured in R group,The resistance training load of each mouse is based on the maximum load value measured each week.Training using the "pyramid" training model,In the order of 50%,75%,100%,75%,50% of the maximum weight of mice,Three,two,one,two,three climbing training sessions;Group rest 1 min,30 s.rest R group of mice measured weekly weight,grip strength;C mice were measured weekly,In weeks 1,4,The maximum load and grip are measured on the time node of week 8.Twelve hours after the last training,10% chloral hydrate anesthesia(3.5 ml/kg body weight),The mice were killed and taken.The quadriceps femoris was fixed in 4%paraformaldehyde solution,Then the histochemical experiments,For HE staining,The cross-sectional area of quadriceps femoris muscle fibers in aging mice was calculated.Take the quadriceps,Changes of Pax7、Myf5、MyoD、CDK4、CDK6、CyclinA2 、 CyclinB1 、 CyclinD3 、 CyclinE2 、 p21 、p16Ink4a protein in mouse quadriceps femoris were detected by Western blotting.Use the IBM SPSS Statistics 23 to carry on the statistical analysis to the data,use the Graphpad Prism8 to carry on the drawing to the experimental data.Results:(1)There was no significant change in body weight in R group during the training period,and the body weight of C group was gradually increased.(2)After the training,the weight of the mice in group C was significantly higher than before the training,the weight of mice in group R was significantly lower than that of mice in group C,and the mass index of quadriceps femoris(quadriceps femoris wet weight/body weight)of mice in group R was significantly higher In group C.(3)During the training period,the maximum weight of the mice in the R group gradually increased and reached the maximum at the 6th week.From the 6th week to the 8th week,the maximum weight decreased slightly;there was no significant change in the maximum weight of the mice in the C group.(4)After the training,the maximum weight of the mice in the R group was significantly higher than that of the C group,and the relative maximum weight(maximum weight/body weight)of the mice in the R group was significantly higher than that of the C group.(5)After the training,the gripping power of the mice in the R group was significantly higher than that of the C group,and the relative gripping power(grip/weight)of the mice in the R group was extremely significantly higher than that of the C group.(6)The average cross-sectional area of quadriceps femoris fibers in R group was significantly larger than that in C group after eight weeks of resistance training.(7)The Pax7 proteins in the R group were significantly up-regulated(P<0.01)and up-regulated(P<0.05).(8)The p21 protein was significantly downregulated(P<0.01)and p16Ink4 a protein significantly downregulated(P<0.05)compared with the C group after 8 weeks of resistance exercise.(9)After 8 weeks of resistance exercise,compared with group C,the expression level of CDK4 protein in group R was extremely significantly reduced(P<0.01),and the expression level of CDK6 protein was significantly reduced(P<0.05);the expression level of CyclinB1 was extremely significant Decrease(P<0.01),CyclinA2,CyclinD3,CyclinE2 protein expression levels were significantly reduced(P<0.05).Conclusions:(1)Aging mice for 8 weeks resistance training can effectively increase the cross section area of quadriceps femoris muscle,improve grip strength and muscle strength.(2)The 8-week anti-impedance training can effectively activate the senescent mouse skeletal muscle satellite cells,promote satellite cells proliferation and differentiation,and facilitate skeletal muscle remodeling.(3)The 8-week resistance exercise can down-regulate the p16Ink4 a protein and release its inhibitory effect on the cyclin kinase of skeletal muscle satellite,down-regulate the p21 protein and release its inhibitory effect on the cyclin-cell cyclin-dependent kinase complex of skeletal muscle satellite,promote satellite cells to enter the cell cycle and alleviate the senescence of satellite cells caused by high p16Ink4a、p21 expression.(4)Skeletal muscle satellite cyclin CyclinA2、CyclinB1、CyclinD3、CyclinE2、down-regulated and cyclin dependent kinase CDK4、CDK6 down-regulated after 8weeks of resistance training.It is assumed that CDKs binds to the Cyclins to form a complex and then play a role in regulating the cell cycle and promoting the satellite cell cycle process of aging mice.Thus,skeletal muscle satellite cells add value. |
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