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目的:探讨中等强度耐力运动对心脏Akt/mTOR信号通路表达的影响及其作用机制。方法:健康雄性SD大鼠40只,随机分为耐力运动组(E组,n=20)和对照组(C组,n=20)。耐力运动组进行8周中等强度跑台训练,建立大鼠耐力运动型心肌肥大模型。使用实时荧光定量PCR技术,对两组大鼠心脏组织Akt、mTOR、eIF4E、p70S6K的mRNA表达进行测定;使用免疫组织化学方法,结合计算机图像处理技术,对心脏组织Akt、mTOR、eIF4E及p70S6K的分布和表达进行观察和测定。结果:8周中等强度耐力训练后,1)E组大鼠心脏组织未见病理性改变。2)E组大鼠心脏组织Akt的mRNA表达未见显著改变(P>0.05),而mTOR、eIF4E、p70S6K的mRNA表达显著上调(P<0.05)。3)E组大鼠心脏组织Akt蛋白免疫反应阳性面积和光密度未发生显著变化(P>0.05),而mTOR、eIF4E及p70S6K蛋白免疫反应阳性面积和光密度显著上调(P<0.05)。结论:1)在中等耐力运动这种特殊的刺激存在时,Akt是mTOR的上游正性调节因子的关系受到抑制,运动刺激直接激活或通过其它途径激活mTOR及其下游因子。2)中等耐力训练导致的耐力型运动心脏的肥大效是由mTOR/p70S6K/eIF4E信号通路直接完成的。3)中等强度耐力训练所致的心脏“生理性肥大”与正常生理发育所致的心脏“生理性肥大”在信号通路的特征上存在差异。
Objective: To investigate the effect of moderate-intensity endurance exercise on the expression of cardiac Akt / mTOR signaling pathway and its mechanism. Methods: Forty healthy male Sprague-Dawley rats were randomly divided into endurance exercise group (group E, n = 20) and control group (group C, n = 20). Endurance exercise group 8 weeks of moderate-intensity treadmill training to establish rat endurance exercise-induced myocardial hypertrophy model. The mRNA expression of Akt, mTOR, eIF4E and p70S6K in cardiac tissue were measured by real-time fluorescence quantitative PCR. The expressions of Akt, mTOR, eIF4E and p70S6K in cardiac tissue were detected by immunohistochemistry and computer image processing Distribution and expression were observed and measured. Results: After 8 weeks of moderate intensity endurance training, there was no pathological change in 1) E group rats heart tissue. 2) There was no significant change in Akt mRNA expression in E group (P> 0.05), while mTOR, eIF4E and p70S6K mRNA levels were significantly increased (P <0.05). 3) There was no significant change in Akt immunoreactive area and optical density in group E (P> 0.05), while the positive area and optical density of protein of mTOR, eIF4E and p70S6K were significantly increased (P <0.05). Conclusions: 1) In the presence of this special stimulus, such as moderate endurance exercise, Akt is inhibited by the upstream positive regulator of mTOR, which stimulates the activation of mTOR and its downstream factors directly or through other pathways. 2) The hypertrophic effect of endurance exercise-induced heart due to moderate endurance training is directly accomplished by the mTOR / p70S6K / eIF4E signaling pathway. 3) There is a difference in the characteristics of the signal pathways between the “physiological hypertrophy” caused by moderate-intensity endurance training and the “physiological hypertrophy” caused by normal physiological development.