大豆肽对力竭运动大鼠血流动力学及心肌自噬水平的影响

Effects of Soybean Peptide on Haemodynamics and Myocardial Autophagy Levels in Rats with Exhaustive Exercise

目的:观察大豆肽对力竭运动大鼠心脏血流动力学及心肌自噬水平的影响,探讨其保护心脏作用的抑制自噬机制。方法:将50只大鼠随机分为:正常对照组(灌胃蒸馏水,不进行强迫运动)、力竭运动模型组(灌胃蒸馏水,并强迫游泳至力竭)、大豆肽高、中、低剂量组(分别灌胃大豆肽500、250及125 mg/kg,并强迫游泳至力竭)。测定麻醉后大鼠左心室LVEDP、LV dp/dt max、LV dp/dt min、LVSP、MABP及HR等参数;取大鼠心尖组织进行HE染色,观察病理组织学改变;取大鼠心肌组织,采用RT-PCR和Western blot法检测心肌组织LC3、Beclin-1及Atg7等因子mRNA和蛋白表达水平。结果:与模型组相比,大豆肽高剂量500 mg可显著降低力竭运动大鼠LVEDP,升高LV dp/dt max、LV dp/dt min、LVSP及MABP,亦可明显改善力竭运动大鼠心肌组织的病理学变化,下调心肌组织LC3、Beclin-1及Atg7 mRNA和蛋白表达水平。结论:大豆肽具有改善力竭运动大鼠心功能和血流动力学的作用,其机制可能与抑制细胞自噬相关。

Objective:To observed the effects of soybean peptide(SP)on haemodynamic and myocardial autophagy levels in rats with exhaustive exercise(EE),its cardioprotective mechanism of inhibiting autophagy was explored. Methods:Fifty rats were divided into 5 groups,normal control group(distilled water by intragastric administration(ig)without compulsive exercise),exhaustive exercise model group,(distilled water by ig,forced swimming to exhaustive),and soybean with high,middle and low dose group(soybean peptide 500,250 and 125 mg/kg by ig,and forced swimming to exhaustive). The rats’ haemodynamic parameers(LVEDP,LV dp/dt max,LV dp/dt min,LVSP,MABP and HR)were measured. The histopathological changes of rats cardiac apex tissue were observed by HE stain. The expression levels of mRNA and protein of LC3,Beclin-1 and Atg7 in myocardial tissue were analyzed by RT-PCR and western blot methods. Results:Compared with the exhausted exercise model group,the LVEDP of the 500 mg/kg SP decreased in rats with exhaustive exercise,the LV dp/dt max,LV dp/dt min,LVSP and MABP increased,improved the hispathological changes of myocardial tissue in rats with exhaustive exercise,down-regulated the expression levels of mRNA and protein of LC3,Beclin-1 and Atg7 in myocardial tissue of rats with exhaustive exercise. Conclusion:Soybean peptide could ameliorate the cardiac function and hemodynamics in rats with exhaustive exercise,and its mechanism may be related to inhibition of autophagy.