摘要
目的:探讨一定周期较大强度耐力运动预处理后大鼠缺血再灌注(I/R)心肌SOD2蛋白表达及其活性变化与心肌保护效应的关系。方法:成年雄性SD大鼠36只,随机分为假手术对照组(A)、心肌缺血再灌注组(B)、较大强度耐力运动+心肌缺血再灌注组(C)。C组在运动干预后与B组一同建立在体I/R(缺血30 min,再灌注60 min)心肌模型。造模过程中观察心电图J点变化,每组选取造模成功者8例进入后续实验。测定血清c Tn I、CK-MB浓度;Western Blotting法测定心肌SOD2蛋白表达水平,测定心肌SOD2、T-SOD活性及MDA含量。结果:B、C组心电图J点、T波值及Q-T间期于心肌缺血30 min时显著增加及延长,而再灌注60 min时的J点基本恢复、T波低平。B组SOD2蛋白表达水平显著高于A组,C组又显著高于B组。造模结束后,B、C组MDA含量及c Tn I、CK-MB浓度显著升高,同时SOD2活性及T-SOD活性显著下降;上述异常变化均以B组更明显。结论:较大强度耐力运动预处理可能通过提高I/R心肌SOD2蛋白表达,缓解SOD2活性下降及活性氧代谢水平升高程度,发挥心脏保护效应。
Objective: This study explored the changes of SOD2 protein expression and activity in rats' cardiac muscle with ischemia reperfusion( I / R) injury after a certain period of vigorous intensity endurance exercise preconditioning,and detected the relationship between their changes and protective effects on myocardial injury. Methods:Thirty-six male adult SD rats were randomly divided into sham-operation control group( A),myocardial ischemia reperfusion group( B),vigorous intensity exercise and myocardial ischemia reperfusion group( C). I / R( 30 min ischemia,60 min reperfusion) myocardial models were established in group C and group B,and J point in ECG map was observed,then 8 rats with successful I / R model in each group were selected into the follow-up experiment. Serum c Tn I,CK-MB were determined,manganese superoxide dismutase 2( SOD2),T-SOD expressions,activities and MDA content were measured by Western blotting. Results: J point,T wave value and Q-T session of ECG in B and C groups increased during 30 min myocardial ischemia,and J point was recovered,T wave was low after 60 min reperfusion. SOD2 expression in B group was higher than in A group while C group's was higher than B group's. After establishing I / R myocardial models,MDA,c Tn I,and CK-MB contents in B and C groups increased significantly while SOD2 and T-SOD activities decreased. The change in B group was higher than in C group. Conclusion: Vigorous intensity endurance exercise preconditioning may protect heart by improving SOD2 expression,alleviating SOD2 activity's decline and active oxygen level in I / R myocardium.
出处
《北京体育大学学报》
CSSCI
北大核心
2014年第11期73-78,共6页
Journal of Beijing Sport University
基金
广西自然科学基金项目(2013GXNSFBA019146)
广西师范大学第一批青年骨干教师成长支持计划项目
