索引超出了数组界限。
[1] 孟丹, 李鹏, 黄雄, 等. 短期和长期运动预适应对力竭大鼠心肌损伤的保护作用[J]. 中国应用生理学杂志, 2017, 33(6):531-534.
[2] 张龙飞, 崔玉娟, 平政, 等. 红景天苷对力竭大鼠心肌线粒体呼吸功能的影响[J]. 解放军医药杂志, 2014, 26(11):1-5,10.
[3] 马宏, 田攀, 李俊峡, 等. 力竭运动和运动预适应对大鼠心脏跨室壁复极离散度和缝隙连接蛋白43影响的研究[J]. 中国循证心血管医学杂志, 2018, 10(3):292-296.
[4] 徐鹏, 康亭, 刘海燕, 等. 力竭运动后不同时相大鼠心电图、心功能变化及Nrf2的作用[J]. 中国应用生理学杂志, 2016, 30(2):146-151.
[5] Ping Z, Zhang LF, Cui YJ, et al. The protective effects of salidroside from exhaustive exercise-induced heart injury by enhancing the PGC-1α-NRF1/NRF2 pathway and mitochondrial respiratory function in rats[J]. Oxid Med Cell Longev, 2015, 2015:876825.
[6] 崔玉娟, 张龙飞, 平政, 等. 红景天苷对力竭大鼠心肌线粒体生物发生关键调控因子的影响[J]. 解放军医药杂志, 2014, 26(11):6-10.
[7] 焦春利, 徐鹏, 曹雪滨. 运动预适应调控力竭运动大鼠NLRP3炎性体信号通路保护心肌的机制研究[J]. 中华危重病急救医学, 2016, 28(7):618-623.
[8] Radovits T, Oláh A, Lux , et al. Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis[J]. Am J Physiol Heart Circ Physiol, 2013, 305(1):H124-H134.
[9] Quindry JC, Hamilton KL. Exercise and cardiac preconditioning against ischemia reperfusion injury[J]. Curr Cardiol Rev, 2013, 9(3):220-229.
[10] French JP, Quindry JC, Falk DJ, et al. Ischemia-reperfusion-induced calpain activation and SERCA2a degradation are attenuated by exercise training and calpain inhibition[J]. Am J Physiol Heart Circ Physiol, 2006, 290(1):H128-H136.
[11] 赵沐霖, 曹雪滨. 运动预适应对力竭大鼠心肌线粒体生物发生及呼吸功能的影响[J]. 中国循环杂志, 2017, 32(z1):50.
[12] 张招, 王洋, 徐鹏, 等. 降钙素基因相关肽参与运动预适应对急性力竭大鼠心脏保护作用的研究[J]. 中华危重病急救医学, 2018, 30(4):369-373.
[13] Frasier CR, Moukdar F, Patel HD, et al. Redox-dependent increases in glutathione reductase and exercise preconditioning: role of NADPH oxidase and mitochondria[J]. Cardiovasc Res, 2013, 98(1):47-55.
[14] Huang CY, Yang AL, Lin YM, et al. Anti-apoptotic and pro-survival effects of exercise training on hypertensive hearts[J]. J Appl Physiol, 2012, 112(5):883-891.
[15] Tsubaki M, Takeda T, Asano RT, et al. Rebamipide suppresses 5-fluorouracil-induced cell death via the activation of Akt/mTOR pathway and regulates the expression of Bcl-2 family proteins[J]. Toxicol In Vitro, 2018, 46:284-293.
[16] Lim SY, Davidson SM, Hausenloy DJ, et al. Preconditioning and postconditioning:the essential role of the mitochondrial permeability transition pore[J]. Cardiovasc Res, 2007, 75(3):530-535.
[17] Zhang H, Xiong ZY, Wang J, et al. Glucagon-like peptide-1 protects cardiomyocytes from advanced oxidation protein product-induced apoptosis via the PI3K/Akt/Bad signaling pathway[J]. Mol Med Rep, 2016, 13(2):1593-1601.
[18] Bopassa JC, Ferrera R, Gateau-Roesch O, et al. PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning[J]. Cardiovasc Res, 2006, 69(1):178-185.
[19] Jie B, Zhang X, Wu X, et al. Neuregulin-1 suppresses cardiomyocyte apoptosis by activating PI3K/Akt and inhibiting mitochondrial permeability transition pore[J]. Mol Cell Biochem, 2012, 370(1/2):35-43.
[20] Rahman S, Li JY, Bopassa JC, et al. Phosphorylation of GSK-3 beta mediates intralipid-induced cardioprotection against ischemia/reperfusion injury[J]. Anesthesiology, 2011, 115(2):242-253.
[21] Zhang J, He Z, Guo J, et al. Sulfiredoxin-1 protects against simulated ischaemia/reperfusion injury in cardiomyocyte by inhibiting PI3K/AKT-regulated mitochondrial apoptotic pathways[J]. Biosci Rep, 2016, 36(2):e00325.
[22] Huang CY, Yang AL, Lin YM, et al. Anti-apoptotic and pro-survival effects of exercise training on hypertensive hearts[J]. J Appl Physiol, 2012, 112(5):883-891.
[23] 谭支内, 蔡梦昕, 陈婷, 等. 间歇运动激活心梗大鼠心肌NRG1-PI3K/Akt通路抑制心肌细胞凋亡[J]. 北京体育大学学报, 2016,39(6):69-76,83.
[24] Yuan Y, Pan SS, Wan DF, et al. H2O2 signaling-triggered PI3K mediates mitochondrial protection to participate in early cardioprotection by exercise preconditioning[J]. Oxid Med Cell Longev, 2018, 2018:1916841.
[25] 刘绍东, 张彦秋, 曹江, 等. 有氧耐力训练对大鼠骨骼肌线粒体功能及PI3K-Akt蛋白的表达影响[J]. 中国应用生理学杂志, 2016, 32(1):55-58.