期刊文献+

不同训练状态大鼠心肌GRP78、GRP94和ERP72的表达 被引量:1

GRP78, GRP94 and ERP72 Expressions in Rat Myocardium of Different Training Status
下载PDF
导出
摘要 探讨运动诱发心肌适应过程中是否有心肌内质网应激的参与。方法:大鼠进行跑台耐力训练,建立不同训练强度、不同训练时间和周期的大鼠运动模型,在末次训练结束后24 h取材,取左室心肌,采用western blot检测内质网应激相关蛋白GRP78、GRP94、ERP72和CHOP的表达。结果:1)5周运动模型组:时间递增组大鼠心肌GRP78较安静组显著升高,GRP94、ERP72、CHOP蛋白表达无显著性差异;恒时恒速组、速度递增组大鼠心肌GRP78、GRP94、ERP72、CHOP蛋白表达较安静组未见显著性差异。2)10周运动模型:恒时恒速组、速度递增组大鼠心肌GRP78、GRP94、ERP72、CHOP蛋白表达较安静组无显著差异。结论:以延长运动持续时间为特征的5周耐力训练诱发GRP78蛋白表达升高,而速度恒定或速度递增的耐力训练没有诱发心肌与内质网应激相关的蛋白表达,提示运动方式可能与心肌内质网应激有关。 Objective: To explore whether endoplasmic reticulum stress is involved in the process of exercise-induced myocardial adaptation. Methods: Rats were subjected to treadmill exercise training with different exercise intensity, duration and exercise program, and then euthanized 24 h after last run. GRP78,GRP94 and ERP72 expressions in myocardium of left ventricular were measured with western blot analysis.Results: 1) there was a significant increase in the GRP78 expression but no significant difference in the expression of GRP94, ERP72, CHOP in duration-increase group. No significant changes in the expression of GRP78, GRP94, ERP72 and CHOP protein expressions in rats undergoing constant speed and speed-increase training were observed in all rats of 5-week trained groups; 2) No significant changes in the expression of GRP78, GRP94, ERP72 and CHOP were observed in all rats of 10-week trained groups when compared with age-matched control group. Conclusion: GRP78 expression was induced in rat myocardium after five-week duration-increase endurance training, while no significant change in GRP78 expression was observed after constant speed or speed-increase training. It suggests that exercise mode might be associated with exercise-induced endoplasmic reticulum stress.
作者 史清钊 陈怡月 王智强 李丁丁 于海燕 姚政立 王蕴红 SHI Qingzhao, CHEN Yiyue, WANG Zhiqiang, LI Dingding, YU Haiyan, YAO Zhengli, WANG Yunhong(Capital University of Physical Education and Sports, Beijing 100191, Chin)
机构地区 首都体育学院
出处 《首都体育学院学报》 CSSCI 北大核心 2018年第3期268-271,281,共5页 Journal of Capital University of Physical Education and Sports
基金 北京市教委项目(KM201310029001 PXM2015_014206_000072 PXM2015_014206_000040)
关键词 运动 心肌 内质网应激 葡萄糖调节蛋白78 exercise cardiac muscle endoplasmic reticulum (ER) glucose-regulated protein 78
  • 相关文献

参考文献3

二级参考文献25

  • 1高俊鹏,蔡定芳.内质网应激介导神经变性疾病错折叠蛋白的神经毒性[J].中国病理生理杂志,2008,24(1):201-205. 被引量:1
  • 2KEMI O J, CECI M, WISLOFF U, et al. Activation or inactivation of cardiac Akt/mTOR signa|ing diverges physiological from patho- logical hypertrophy[J]. J Cell Physiol, 2008(214) .. 316.
  • 3HETZ C. The unfolded protein response., controlling cell fate deci- sions under ER stress and beyond[J]. Nat Rev Mol Cell Bid, 2012, 13(2) ..89.
  • 4KIM I, XU W, BEED J C. Cell death and endoplasmic reticulum stress:disease relevance and therapeutic opportunlties[-J~. Nat Rev Mol Cell Biol, 2008,7(12) : 101K.
  • 5PEREIRA B C,DA ROCHA A L,PINTO A P, et al. Excessive ec- centric exercise-induced overtraining model leads to endoplasmlc re- ticulum stressin mice skeletal muscles[J]. Life Sci, 2016(145) .. 144.
  • 6DIANE R F, CONSTANTANTINOS K. The PERK-elF2a-ATF4 module of the UPR in hypoxia resistance and tumor growth[-J~. Cancer Biol Ther, 2006,5 (7) .. 723.
  • 7BEDFORD T G,TIPTON C M,WILSON N C,et al. Maximum ox- ygen consumption of rats and its changes with various experimental procedures[J]. J Appl Physiol 1979(47):1278.
  • 8MURLASITS Z, LEE Y, POWERS S K. Short-term exercise does not increase ER stress protein expression in cardiac muscle[J]. Med Sci Sports Exerc , 2007,39 (9) .. 1522.
  • 9OST M, COLEMAN V, KASCH J, et al. Regulation of myokine expression: Role of exercise and cellular stressEJ']. Free Radical Bi- ology and Medicine ,2016(2) :17.
  • 10LIU Z W, ZHU H T, CHEN K L, et al. Protein kinase RNA-like endoplasmic reticulum kinase (PERK) signaling pathway plays a major role in reactive oxygen species (ROS)-mediated endoplasmic reticulum stress-induced apoptosis in diabetic cardiomyopathy[-J~. Cardiovasc Diabetol, 2013 (12) .- 158.

共引文献47

同被引文献1

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部