Department of Applied Physiology and Kinesiology, Center for Exercise Science, University of Florida, Gainesville, FL 32611, USA.
J Physiol Sci. 2010 May;60(3):181-6. doi: 10.1007/s12576-009-0082-2. Epub 2010 Jan 7.
Increased myocardial cyclooxygenase-2 (COX-2) activity is essential for late phase ischemic preconditioning (IPC). Currently unknown is whether cardioprotection elicited by exercise also involves elevated myocardial COX-2 activity. This investigation tested whether aerobic exercise elevates myocardial COX-2 protein content or enzyme activity in young and senescent male Fisher 344 rats assigned to sedentary or cardioprotective endurance exercise treatments (3 consecutive days of treadmill exercise, 60 min/day @ approximately 70% VO(2)max). Assay of cardiac COX-2 protein content, catalytic activity, and inducible nitric oxide synthase (iNOS) protein content reveal that exercise did not alter COX-2 activity (PGE(2), p = 0.866; PGF1alpha, p = 0.796) or protein levels (p = 0.397) within young or senescent hearts. In contrast, myocardial iNOS, an up-stream mediator of COX-2 expression, was over-expressed by an average of 37% in aged hearts (p = 0.005), though iNOS was not influenced by exercise. Findings reveal exercise does not elevate cardiac COX-2 activity and suggests that mechanisms responsible for cardioprotection differ between IPC and aerobic exercise.
心肌环氧化酶-2(COX-2)活性增加对于晚期缺血预处理(IPC)是必要的。目前尚不清楚运动引起的心脏保护是否也涉及心肌 COX-2 活性的升高。本研究旨在检测有氧运动是否会增加年轻和衰老雄性 Fisher 344 大鼠的心肌 COX-2 蛋白含量或酶活性,这些大鼠被分配到久坐或保护性耐力运动治疗组(连续 3 天进行跑步机运动,每天 60 分钟,约 70% VO2max)。心脏 COX-2 蛋白含量、催化活性和诱导型一氧化氮合酶(iNOS)蛋白含量的测定表明,运动并没有改变年轻或衰老心脏中的 COX-2 活性(PGE2,p=0.866;PGF1alpha,p=0.796)或蛋白水平(p=0.397)。相比之下,心肌 iNOS 是 COX-2 表达的上游调节剂,在衰老心脏中平均过度表达 37%(p=0.005),尽管运动并没有影响 iNOS。研究结果表明,运动不会增加心脏 COX-2 活性,并表明 IPC 和有氧运动之间的心脏保护机制不同。