BACKGROUND:Several studies have demonstrated that JAK2 kinase plays an important role in myocardial protection by ischemic preconditioning and medicine preconditioning. OBJECTIVE:To investigate the effects of exercise preconditioning on JAK2 mRNA and protein expression in the rat heart and the underlying mechanism of action. METHODS:SD rats were randomly divided into control, exhaustive, exercise preconditioning, and exercise preconditioning + AG490 groups. Rats in the control and exhaustive groups were fed routinely for 3 days. Rats in the exercise preconditioning and exercise preconditioning + AG490 groups were subjected to intermittent treadmil exercise for 3 successive days to establish exercise preconditioning animal models. Rats in the exercise preconditioning + AG490 group were intraperitonealy injected with JAK2 inhibitor AG490 at 10 minutes before exercise preconditioning. After 3 days, rats in the exhaustive, exercise preconditioning, and exercise preconditioning + AG490 groups were subjected to exhaustive treadmil exercise. Serum levels of lactate dehydrogenase and creatine kinase isoenzyme were determined. JAK2 mRNA and protein expression in the rat myocardial tissue was detected by real-time fluorescent quantitative PCR and immunohistochemistry.RESULTS AND CONCLUSION:Compared with the control group, serum levels of actate dehydrogenase and creatine kinase isoenzyme were increased, and JAK2 mRNA and protein expression in the myocardial tissue was significantly increased in the exhaustive group (P < 0.05). Compared with the exhaustive group, serum levels of actate dehydrogenase and creatine kinase isoenzyme were decreased (P < 0.05), while JAK2 mRNA and protein expression in the myocardial tissue was increased in the exercise preconditioning group (P < 0.05). Compared with the exercise preconditioning group, serum levels of actate dehydrogenase and creatine kinase isoenzyme were increased (P < 0.05), while JAK2 mRNA and protein expression in the myocardial tissue was decreased in the exercise preconditioning + AG490 group (P < 0.05). The results confirm that exercise preconditioning plays its cardioprotective role through activating JAK/STAT signaling pathway, up-regulating the expression of JAK2 mRNA and protein in the cardiac tissue and aleviating myocardial ischemia injury.%背景:研究表明JAK2激酶在缺血预适应和药物预适应的心肌保护机制中发挥重要作用.目的:观察运动预适应模型大鼠心脏JAK2 mRNA和蛋白表达的影响及其对心脏保护的作用机制.方法:将 SD 大鼠随机分为对照组、力竭组、运动预适应组、运动预适应+AG490 组.对照组和力竭组大鼠常规饲养3 d;运动预适应组和运动预适应+AG490组大鼠进行连续3 d的间歇跑台运动建立运动预适应动物模型,后一组在运动预适应前10 min腹腔注射JAK2抑制剂AG490.3 d后,力竭组、运动预适应组和运动预适应+AG490 组进行一次性力竭跑台运动.观察血清乳酸脱氢酶和肌酸激酶同工酶的活性,用实时荧光定量PCR和免疫组织化学方法检测心脏JAK2 mRNA和蛋白的表达.结果与结论:与对照组相比,力竭组血清乳酸脱氢酶和肌酸激酶同工酶活性增加,心脏JAK2 mRNA和蛋白的表达升高(P < 0.05);与力竭组相比,运动预适应组血清乳酸脱氢酶和肌酸激酶同工酶活性降低(P < 0.05),心脏JAK2 mRNA和蛋白表达升高(P< 0.05);与运动预适应组相比,运动预适应+AG490组血清乳酸脱氢酶和肌酸激酶同工酶活性增加(P < 0.05),心脏JAK2 mRNA和蛋白的表达降低(P < 0.05).结果证实,运动预适应通过激活JAK/STAT信号通路,上调心脏JAK2 mRNA表达,增加心脏JAK2蛋白合成,减轻心肌缺血损伤,从而发挥其心脏保护作用.
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