体育科学
體育科學
체육과학
China Sport Science
2014年
10期
72~77
,共null页
TGFβ通路 少肌症 D-半乳糖 运动 鼠 动物实验
TGFβ通路 少肌癥 D-半乳糖 運動 鼠 動物實驗
TGFβ통로 소기증 D-반유당 운동 서 동물실험
TGFβ; pathway; sarcopenia; D-Glactose; exercise; rat; animal experiment
目的:研究TGFβ(经典和非经典)通路在运动缓解衰老性肌肉流失(少肌症)中的作用。方法:24只雄性Wistar大鼠分为3组,C组(青年安静组)、S组(40dD-半乳糖注射致衰老组)、E组(40dD-半乳糖注射+6wk跑台运动的衰老运动组)。检测各组大鼠体重、腓肠肌重量、TGFβ(经典与非经典)通路因子——TGFβ1、MSTN、Phospho-smad2/3、PhosphoMAPKs(p38、JNK1/2、ERK1/2)及通路效应因子——p21、Pax7(WB法)、MyoD mRNA、MyoG mRNA(RT-PCR法)。结果:与C组相比,S组腓肠肌比重(腓肠肌重量/体重)降低,TGFβ1、MSTN、Phospho-smad2/3、Phospho-MAPKs(Phospho-p38、Phospho-JNK1/2、PhosphoERK1/2)、p21、MyoD mRNA、MyoG mRNA升高,Pax7降低;与S组相比,E组腓肠肌比重升高,TGFβ1、MSTN、Phospho-smad2/3、Phospho-MAPKs(Phospho-JNK1/2、Phospho-ERK1/2)降低,p21、Pax7、MyoD mRNA、MyoG mRNA升高。结论:运动训练抑制了TGFβ经典及非经典通路并缓解了衰老肌肉的流失,Pax7、p21、MyoD、MyoG可能作为TGFβ通路的效应器介导了该过程。
目的:研究TGFβ(經典和非經典)通路在運動緩解衰老性肌肉流失(少肌癥)中的作用。方法:24隻雄性Wistar大鼠分為3組,C組(青年安靜組)、S組(40dD-半乳糖註射緻衰老組)、E組(40dD-半乳糖註射+6wk跑檯運動的衰老運動組)。檢測各組大鼠體重、腓腸肌重量、TGFβ(經典與非經典)通路因子——TGFβ1、MSTN、Phospho-smad2/3、PhosphoMAPKs(p38、JNK1/2、ERK1/2)及通路效應因子——p21、Pax7(WB法)、MyoD mRNA、MyoG mRNA(RT-PCR法)。結果:與C組相比,S組腓腸肌比重(腓腸肌重量/體重)降低,TGFβ1、MSTN、Phospho-smad2/3、Phospho-MAPKs(Phospho-p38、Phospho-JNK1/2、PhosphoERK1/2)、p21、MyoD mRNA、MyoG mRNA升高,Pax7降低;與S組相比,E組腓腸肌比重升高,TGFβ1、MSTN、Phospho-smad2/3、Phospho-MAPKs(Phospho-JNK1/2、Phospho-ERK1/2)降低,p21、Pax7、MyoD mRNA、MyoG mRNA升高。結論:運動訓練抑製瞭TGFβ經典及非經典通路併緩解瞭衰老肌肉的流失,Pax7、p21、MyoD、MyoG可能作為TGFβ通路的效應器介導瞭該過程。
목적:연구TGFβ(경전화비경전)통로재운동완해쇠로성기육류실(소기증)중적작용。방법:24지웅성Wistar대서분위3조,C조(청년안정조)、S조(40dD-반유당주사치쇠로조)、E조(40dD-반유당주사+6wk포태운동적쇠로운동조)。검측각조대서체중、비장기중량、TGFβ(경전여비경전)통로인자——TGFβ1、MSTN、Phospho-smad2/3、PhosphoMAPKs(p38、JNK1/2、ERK1/2)급통로효응인자——p21、Pax7(WB법)、MyoD mRNA、MyoG mRNA(RT-PCR법)。결과:여C조상비,S조비장기비중(비장기중량/체중)강저,TGFβ1、MSTN、Phospho-smad2/3、Phospho-MAPKs(Phospho-p38、Phospho-JNK1/2、PhosphoERK1/2)、p21、MyoD mRNA、MyoG mRNA승고,Pax7강저;여S조상비,E조비장기비중승고,TGFβ1、MSTN、Phospho-smad2/3、Phospho-MAPKs(Phospho-JNK1/2、Phospho-ERK1/2)강저,p21、Pax7、MyoD mRNA、MyoG mRNA승고。결론:운동훈련억제료TGFβ경전급비경전통로병완해료쇠로기육적류실,Pax7、p21、MyoD、MyoG가능작위TGFβ통로적효응기개도료해과정。
Objectvie:To explore the functions of(canonical and uncanonical)TGFβpathway in exercise-induced improvement of sarcopenia.Method:24 male wistar rats were divided into 3groups:C group(quiet young group),S group(40day D-Glactose injection-induced senecence),E group(40days D-Glactose injection-induced senecence+6weeks exercise trainning on treadmill).To detect body wet weight,gastrocnemius wet weight(by weighment),TGFβpathway component-TGFβ1,MSTN,Phospho-smad2/3,Phospho-MAPK(p38,JNK1/2,ERK1/2),TGFβpathway effector-p21,Pax7 by WB and MyoD mRNA,MyoG mRNA by RT-PCR in each group.Result:The ratio of gastrocnemius weight to body weight decreased,but TGFβ1,MSTN,Phospho-smad2,3,Phospho-p38,Phospho-JNK1,2,Phospho-ERK1,2,p21,MyoD mRNA,MyoG mRNA increased and Pax7 decreased in S group vs C group.The ratio of gastrocnemius weight to body weight increased,but TGFβ1,MSTN,Phospho-smad2,3,Phospho-JNK1,2,Phospho-ERK1,2decreased,Phospho-p38 unchanged,and p21,Pax7,MyoD mRNA,MyoG mRNA increased in E group vs S group.Conclusion:Exericse trainning can improve senescene-induced muscle loss by inhibiting TGFβcanonical and uncanonical pathway with the mediation of Pax7,p21,MyoD and MyoG.