nav emailalert searchbtn searchbox tablepage yinyongbenwen piczone journalimg journalInfo journalinfonormal searchdiv searchzone qikanlogo popupnotification paper paperNew
2009, 04, v.24;No.v.24 334-336+365
抗阻训练对衰老小鼠心肌Sarcopenia中Akt/mTOR信号通路的影响
基金项目(Foundation):
邮箱(Email):
DOI:
摘要:

目的:探讨抗阻训练对衰老小鼠心肌sarcopenia中Akt/mTOR信号通路的影响。方法:雄性,3月龄SAMP8小鼠随机分为对照组(n=12)和抗阻训练组(n=12)。对照组常规喂养至6月龄,达到衰老后处死;抗阻训练组进行3个月的抗阻训练,建立衰老小鼠抗阻训练运动模型,使用实时荧光定量PCR技术,对小鼠心肌Akt/mTOR信号通路中Akt、mTOR、p70S6K和eIF-4E基因mRNA的表达进行测定。结果:衰老小鼠出现心肌纤维数目减少,心肌纤维空白区域面积增多;抗阻训练后,小鼠心脏重量和心系数与衰老对照组相比虽然显著增加(P<0.05)但没有产生病理性心肌肥大;心肌纤维空白区域面积小于对照组;抗阻训练组Akt、mTOR、p70S6K和eIF-4E基因mRNA的表达与衰老对照组相比显著上升(P<0.05)。结论:抗阻训练可以增强衰老小鼠心肌Akt/mTOR信号通路中各基因mRNA的表达,产生运动性心肌肥大,并对心肌产生保护性调节作用,改善衰老小鼠的心脏功能。

Abstract:

Objective:To study the effect of resistance training on cardiac sarcopenia.Methods:Male SAMP8 3-months old mice were randomly divided into control group(n=12)and resistance training group(n=12).The control group was executed at 6-months old.After inducing the animal model of resis-tance training,using the realtime PCR system to analyze the mRNA expression of Akt,mTOR,p70S6K and eIF-4E in mouse heart.Result:The aging mice turned cardiac sarcopenia.After resistance training,the mouse heart weight and the ventricular mess index significantly increased(P<0.05),without pathological cardiac hypertrophy,and did not turn cardiac sarcopenia.The mRNA expressions of Akt,mTOR,p70S6K and eIF-4E of resistance training group increased significantly than that of the aging control group(P<0.05).Conclusion:The resistance training can elevate the cardiac PI3-K/Akt signaling pathway expression,induce exercise cardiac hypertrophy,start the cardiac cell protection control action,and improve the cardiac function of aging mice.

参考文献

[1]Jing Lin,Elizabeth F Lopez,Jin Yufang,et al.Age-related cardiacmuscle sarcopenia:Combining experimental and mathematical modelingto identify mechanisms[J].Experimental Gerontology,2008,43(4):296-306.

[2]Kotulska K,Larysz-Brysz M,Grajkowska W,et al.Cardiac rhabdomyomasin tuberous sclerosis complex showapoptosis regulation and mTOR pathwayabnormalities[J].Pediatr Dev Pathol,2009,12(2):89-95.

[3]Kemi O J,Ceci M,Wisloff U,et al.Activation or inactivation of cardiacAkt/mTOR signaling diverges physiological from pathological hypertrophy[J].Cell Physiol,2008,214(2):316-21.

[4]ValérioG,Barauna,Kaleizu T,et al.AT1 receptor participates inresistance training-induced cardiac hypertrophy in rats[J].Molecular andCellular Cardiology,2007,42(6):S138.

[5]Sukho Lee R P Farrar.Resistance training induces muscle-specificchanges in muscle mass and function in rat[J].Journal of ExercisePhysiolog,2003,6:80-87.

[6]Livak K J,Schmittgen T D.Analysis of relative gene expression data usingreal-time quantitative PCR and the 2(-Delta Delta CT)method[J].Methods,2001,25(4):402-408.

[7]Siu P M,Bryber R W,Martyn J K,et al.Apoptotic adaptations fromexercise training in skeletal and cardiac muscles[J].FASEB,2004,8(10):1150-1152.

[8]Solange M,Franzói-De-Moraes,S B Peres,et al.The Akt/PKBphosphorylation in cardiac muscle is modulated by an exercise trainingprogram[J].Diabetes Research and Clinical Practice,2000,50:375.

[9]Li W,Tan D,Zhang Z,et al.Activation of Akt-mTOR-p70S6K pathwayin angiogenesis in hepatocellular carcinoma[J].Oncol Rep,2008,20(4):713-9.

[10]Dreyer H C,Glynn E L,Lujan H L,et al.Chronic paraplegia-inducedmuscle atrophy down regulates the mTOR/S6K1 signaling pathway[J].JAppl Physiol,2008,104(1):27-33.

[11]Fluckey J D,Knox M,Smith L,et al.Insulin-facilitated increase of muscle protein synthesis after resistance exercise involves a MAP kinasepathway[J].Am J Physiol Endocrinol Metad,2006,290(6):E1 205-1211.

[12]Kubica N,Bolster D R,Farrell P A,et al.Resistance exercise increases muscle protein synthesis and translation of eukaryotic initiation factor 2Bepsilon mRNA in a mammalian target of rapamycin-dependent manner[J].J Biol Chem,2005,280(9):7 570-7 580.

[13]Hanada M,Feng H,Hemmings BA.Structure regulation and function of PKB/AKT major therapeutic target[J].Biochim Biophysica Acta,2004,1697:3 216.

[14]Montagne J,Stewart M J,Stocker H,et al.Drosophila S6 kinase:Aregulator of cell size[J].Sci,1999,285:2 126-2 129.

[15]Lou H,Danelisen I,Singal P K.Involvement of mitogen-activated protein kinases in adriamycin-induced cardiomyopathy[J].Am J PhysiolHeart Circ Physiol,2005,288(4):H1 925-30.

基本信息:

中图分类号:G804.7

引用信息:

[1]李欣,丁树哲,卢健.抗阻训练对衰老小鼠心肌Sarcopenia中Akt/mTOR信号通路的影响[J].天津体育学院学报,2009,24(04):334-336+365.

发布时间:

2009-07-25

出版时间:

2009-07-25

检 索 高级检索

引用

GB/T 7714-2015 格式引文
MLA格式引文
APA格式引文