Ashraf Javad, Roshan Valiollah Dabidi
Department of Sport Physiology, College of Physical Education and Sport Sciences, University of Mazandaran, Babolsar, Iran.
Asian Pac J Cancer Prev. 2012;13(8):4025-30.
Cardiotoxicity and oxidative stress is a life-threatening side effect of doxorubicin (DOX). We investigate the effects of short-term exercise as therapeutic tool for improvement of cardioprotection against DOX-induced cardiotoxicity in the rat.
Wistar males (weighing 257 ± 28 g) were divided into six groups: (1) control+placebo (2) control+DOX 10 mg.kg(-1) (3) control+DOX 20mg.kg(-1) (4) training+placebo (5) training+ DOX10 mg.kg(-1) (6) training+DOX 20mg.kg(-1). Cardiotoxicity was induced by DOX (10 and 20 mg.kg(-1)). The rats in groups 4, 5 and 6 experienced treadmill running of 25 to 39 min.day(-1) and 15 to 17 m.min(-1), 5 days/ wk for 3 wk. At the end of the endurance training program, rats in the 1 and 4 groups, in the 2 and 5 groups and in the 3 and 6 groups received saline solution, DOX 10 mg.kg(-1) and DOX 20 mg.kg(-1), respectively.
DOX administration (10 and 20 mg.kg(-1)) caused significant increase in MDA and Apelin, an insignificant increase in NO and a significant decrease in SOD, as compared to the C+P group. Three weeks of the pretreatment endurance exercise resulted in a significant increase of Apelin and SOD, an insignificant increase of NO and an insignificant decrease of MDA, as compared to the C+P group. Furthermore, after three weeks of endurance training and DOX treatment with 10mg.kg(-1) and 20mg.kg(-1), a significant increase in apelin and SOD, and a significant decrease in MDA were detected in comparison to C+DOX10 and/or C+DOX20 groups. There was a significant difference between DOX10 mg.kg(-1) and DOX20 mg.kg(-1) treatments in MDA levels only.
Pretreatment exercise may improve myocardial tolerance to DOX-induced cardiotoxicity by inhibition of oxidative stress and up- regulation of antioxidants in heart tissue.
心脏毒性和氧化应激是阿霉素（DOX）一种危及生命的副作用。我们研究短期运动作为一种治疗手段对改善大鼠抗DOX诱导的心脏毒性的心脏保护作用。
将雄性Wistar大鼠（体重257±28g）分为六组：（1）对照组+安慰剂组；（2）对照组+10mg.kg⁻¹ DOX组；（3）对照组+20mg.kg⁻¹ DOX组；（4）训练组+安慰剂组；（5）训练组+10mg.kg⁻¹ DOX组；（6）训练组+20mg.kg⁻¹ DOX组。DOX（10和20mg.kg⁻¹）诱导心脏毒性。第4、5和6组的大鼠每天在跑步机上以15至17米/分钟的速度跑25至39分钟，每周5天，共3周。在耐力训练计划结束时，第1和4组、第2和5组、第3和6组的大鼠分别接受生理盐水、1mg.kg⁻¹ DOX和20mg.kg⁻¹ DOX。
与对照组+安慰剂组相比，给予DOX（10和20mg.kg⁻¹）导致丙二醛（MDA）和Apelin显著增加，一氧化氮（NO）略有增加，超氧化物歧化酶（SOD）显著降低。与对照组+安慰剂组相比*，三周的预处理耐力运动导致Apelin和SOD显著增加，NO略有增加，MDA略有降低。此外，在进行三周的耐力训练并用10mg.kg⁻¹和20mg.kg⁻¹ DOX治疗后，与对照组+10mg.kg⁻¹ DOX和/或对照组+20mg.kg⁻¹ DOX组相比，检测到Apelin和SOD显著增加，*MDA显著降低。仅在MDA水平上，10mg.kg⁻¹ DOX和20mg.kg⁻¹ DOX治疗之间存在显著差异。
预处理运动可能通过抑制氧化应激和上调心脏组织中的抗氧化剂来提高心肌对DOX诱导的心脏毒性的耐受性。
