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运动诱导的心肌肥大中mTOR信号通路的调控

Regulation of mTOR Pathway in Exercise-induced Cardiac Hypertrophy.

作者信息

Liao J, Li Y, Zeng F, Wu Y

机构信息

Department of Sport Science, Beijing Sport University, Beijing, China.

Department of Sport, Jianghan University, Wuhan, China.

出版信息

Int J Sports Med. 2015 May;36(5):343-50. doi: 10.1055/s-0034-1395585. Epub 2015 Jan 21.

Abstract

This study was designed to examine whether the mTOR signaling pathway would respond to long-term different intensity exercises and to observe the impact of exercise upon possible cardiac damage. Male Sprague Dawley rats were randomly divided into control group, moderate-intensity exercise group and high-intensity exercise group, and each exercise group had 4 observation time points (1-24 h). Exercise training lasted 8 weeks with a 2-day break for each week. Serum cTnI was measured by ELSIA and myocardium histology was assessed by HE and HBFP. The expressions of Akt, mTOR, p70(S6K) and their phosphorylated forms were determined by western-blot. Both exercises were effective at inducing cardiac hypertrophy, wherein magnitude increased with exercise intensity. The significantly high level of serum cTnI in the high-intensity group was accompanied by obvious myocellular abnormalities and ischemia in the myocardium. Significant activation of Akt, mTOR and p70(S6K) were observed in the moderate exercise group but not in the high-intensity exercise group. Results indicate that long-term high-intensity exercise training would induce cardiac hypertrophy accompanied by damage to the heart, entailing a risk of pathological changes. There might be a pivotal regulatory role of the mTOR signaling pathway on cardiac hypertrophy after long-term moderate exercise, but not after high-intensity exercise.

摘要

本研究旨在探讨mTOR信号通路是否会对长期不同强度的运动产生反应,并观察运动对可能的心脏损伤的影响。将雄性Sprague Dawley大鼠随机分为对照组、中等强度运动组和高强度运动组,每个运动组有4个观察时间点(1 - 24小时)。运动训练持续8周,每周休息2天。通过酶联免疫吸附测定法(ELSIA)检测血清肌钙蛋白I(cTnI),并通过苏木精-伊红(HE)和苏木精-碱性品红-甲醛(HBFP)评估心肌组织学。通过蛋白质免疫印迹法测定Akt、mTOR、p70(S6K)及其磷酸化形式的表达。两种运动均能有效诱导心脏肥大,其程度随运动强度增加而增加。高强度组血清cTnI水平显著升高,同时伴有明显的心肌细胞异常和心肌缺血。在中等强度运动组中观察到Akt、mTOR和p70(S6K)的显著激活,而在高强度运动组中未观察到。结果表明,长期高强度运动训练会诱导心脏肥大并伴有心脏损伤,存在病理变化的风险。mTOR信号通路可能对长期中等强度运动后的心脏肥大起关键调节作用,但对高强度运动后则不然。

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