College of Life Sciences, Institute of Sports and Exercise Biology, Shaanxi Normal University, No. 620, West Chang'an Avenue, Chang'an District, Xi'an, 710119, Shaanxi, People's Republic of China.
Appl Biochem Biotechnol. 2019 Mar;187(3):663-676. doi: 10.1007/s12010-018-2841-0. Epub 2018 Jul 23.
It has been reported that hydrogen-rich saline (HRS) water reduces oxidative stress, and early aerobic exercise (eAE) acts an efficient exercise preconditioning (EP) against cardiac I/R injury. However, whether early aerobic exercise combined with hydrogen-rich saline (eAE-HRS) water can more effectively protect myocardial damage induced by acute myocardial infarction (MI) is still unknown. This study was aimed to evaluate the effect of eAE-HRS in preventing MI-induced myocardial damage and explore the possible underlying mechanisms. After Sprague-Dawley (SD) rats were given a intragastric administration of HRS (1.6 ppm) at a dosage of 10 mL/kg weight daily for 3 weeks and/or the SD rats were performed a eAE program with 3 weeks running training, the left anterior descending coronary artery was ligated to induce MI. We assessed the effects of eAE-HRS on myocardial injury and oxidative damage in the MI model of rats and detected the effects of eAE-HRS on the expressions of cardiac OGG1 and Tom40, Tom20, and Tim23. The eAE-HRS increased significantly left ventricular systolic pressure, reduced left ventricular end-diastolic pressure, and potentiated + dp/dt, -dp/dt, heart coefficient and pH after MI injury. The eAE-HRS reduced MI-induced CK-MB level, c-Tnl level, h-FABP level, infarct size. The eAE-HRS enhanced MI-induced levels of the superoxide dismutase and total antioxidant capacity, attenuated MI-induced levels of malondialdehyde and catalase. The eAE-HRS increased expressions of OGG1, Tom20 and Tim23 proteins after MI injury, but not Tom40. The eAE-HRS has the potential to be a novel precautionary measure to protect myocardial injury after MI via partially regulating expressions of antioxidant-related proteins and mitochondrial-associated proteins.
据报道，富氢盐水（HRS）可减轻氧化应激，早期有氧运动（eAE）是一种有效的心脏缺血再灌注损伤（I/R）的运动预处理（EP）。然而，早期有氧运动联合富氢盐水（eAE-HRS）是否能更有效地保护急性心肌梗死（MI）引起的心肌损伤尚不清楚。本研究旨在评估 eAE-HRS 预防 MI 诱导的心肌损伤的效果，并探讨其可能的潜在机制。在 Sprague-Dawley（SD）大鼠给予 10ml/kg 体重的 1.6ppm HRS 灌胃 3 周，或 SD 大鼠进行 3 周跑步训练的 eAE 方案后，结扎左前降支冠状动脉诱导 MI。我们评估了 eAE-HRS 对 MI 模型大鼠心肌损伤和氧化损伤的影响，并检测了 eAE-HRS 对心脏 OGG1 和 Tom40、Tom20 和 Tim23 表达的影响。eAE-HRS 可明显增加左心室收缩压，降低左心室舒张末期压，增强+dp/dt、-dp/dt、心脏系数和 pH 值。eAE-HRS 降低了 MI 诱导的 CK-MB 水平、c-Tnl 水平、h-FABP 水平、梗死面积。eAE-HRS 增强了 MI 诱导的超氧化物歧化酶和总抗氧化能力水平，减轻了 MI 诱导的丙二醛和过氧化氢酶水平。eAE-HRS 增加了 MI 后 OGG1、Tom20 和 Tim23 蛋白的表达，但 Tom40 蛋白的表达没有增加。eAE-HRS 可能通过部分调节抗氧化相关蛋白和线粒体相关蛋白的表达，成为预防 MI 后心肌损伤的一种新的预防措施。
