Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran; Department of Exercise Physiology, Faculty of Sport Sciences, University of Guilan, Rasht, Iran.
Department of Exercise Physiology, Faculty of Sport Sciences, University of Guilan, Rasht, Iran.
Life Sci. 2018 Nov 15;213:102-108. doi: 10.1016/j.lfs.2018.10.035. Epub 2018 Oct 22.
Ischemia-reperfusion injury is one of the most common cardiac disorders leading to irreversible heart damage. Many underlying mechanisms seem to be involved, among which mitochondrial dysfunction. Since physical training has a beneficial effect on mitochondrial dynamics (fusion and fission), it may have a cardioprotective effect against IR injury also via mitochondrial pathways. This study investigates the protective role of aerobic training against cardiac IR injury and the mitochondrial dynamics as a possible mechanism.
Thirty-two male Wistar rats (8-week old) were divided into a control, sham, control + IR, and training + IR groups (8 rats each). Training group was exercised aerobically on a treadmill for 8 weeks (5 days/week). After 8 weeks, anesthetized rats underwent a left thoracotomy (sham, control + IR, and training + IR groups) to access the left anterior descending coronary artery, which was occluded by a silk suture for 30 min and released for 90 min of reperfusion (IR groups). Triphenyltetrazolium chloride staining was used to determine the infarct size. The gene expression of mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and dynamin-related protein 1 (Drp1) was evaluated by RT-PCR. A one-way ANOVA was used for statistical analysis with the significance level set at P ≤ 0.05.
Cardiac infarct size was smaller In training + IR group (20.24 ± 5.7%) than in control + IR (35.9 ± 2.3%; P ≤ 0.05). Training + IR showed higher expression of Mfn1 and Mfn2 (P ≤ 0.05). Conversely, Drp1 expression was lower after training (P ≤ 0.05).
Exercise-induced regulation of mitochondrial fusion and fission, leading to improvement of mitochondrial dynamics seems to be involved in the cardioprotection against IR injuries.
缺血再灌注损伤是导致不可逆性心脏损伤的最常见心脏疾病之一。许多潜在机制似乎都与之相关，其中包括线粒体功能障碍。由于体育锻炼对线粒体动力学（融合和分裂）有有益的影响，因此它可能通过线粒体途径对 IR 损伤具有心脏保护作用。本研究旨在探讨有氧训练对心脏 IR 损伤的保护作用及其作为可能机制的线粒体动力学。
32 只 8 周龄雄性 Wistar 大鼠被分为对照组、假手术组、对照组+IR 组和训练组+IR 组（每组 8 只）。训练组在跑步机上进行 8 周的有氧运动（每周 5 天）。8 周后，麻醉大鼠进行左开胸术（假手术组、对照组+IR 组和训练组+IR 组）以进入左前降支冠状动脉，用丝线缝线将其闭塞 30 分钟，然后再恢复灌注 90 分钟（IR 组）。氯化三苯基四氮唑染色用于确定梗死面积。通过 RT-PCR 评估融合蛋白 1（Mfn1）、融合蛋白 2（Mfn2）和动力相关蛋白 1（Drp1）的基因表达。采用单因素方差分析进行统计分析，显著性水平设为 P≤0.05。
与对照组+IR 组（35.9±2.3%）相比，训练组+IR 组的心脏梗死面积更小（20.24±5.7%；P≤0.05）。训练组+IR 组 Mfn1 和 Mfn2 的表达更高（P≤0.05）。相反，训练后 Drp1 的表达降低（P≤0.05）。
运动诱导的线粒体融合和分裂的调节，导致线粒体动力学的改善，可能与 IR 损伤的心脏保护作用有关。
