AMPKα2基因缺乏对小鼠运动性心肌肥厚的影响

发布时间：2018-03-23 20:38

本文选题：运动性心肌肥厚　切入点：AMPKα2　出处：《上海体育学院》2017年硕士论文

【摘要】：研究目的通过对AMPKα2基因敲除小鼠进行跑台运动,探讨AMPK α 2在运动性心肌肥厚中的作用机制。研究方法成年雄性AMPK α 2 KO(KO))小鼠和野生型对照小鼠(WT)各18只,随机分为运动组(EX)和对照组(Ctr),即 WT+Ctr(n=6)、WT+EX(n=12)、KO+Ctr(n=6)和 KO+EX(n=12)。WT+EX和KO+EX进行长期的跑台运动训练以建立运动性心肌肥厚模型。心脏超声检测小鼠心功能和形态等指标,苦味酸-天狼猩红染色检测心肌纤维化,WGA染色计算心肌细胞大小,免疫蛋白印记法检测心肌相关蛋白表达情况。研究结果1.超声结果显示,基础状态下,WT+Ctr、WT+EX、KO+Ctr和K0+EX各组小鼠心脏超声结果并没有显著性差异(p0.05)。7周跑台运动后,WT+EX和K0+EX小鼠较各自对照组小鼠EF值有增高的趋势,但尚未见显著性差异(p0.05);WT+EX和KO+EX组收缩末期室间隔厚度(IVS;S)较各自对照组都有显著提高(p0.05)。WT+EX组较WT+Ctr组比,FS有显著增高(p0.05)。K0+EX组小鼠左室收缩末期室壁厚度([VPW;S)显著大于WT+EX(p0.05)。2.安静状态下,AMPK α 2基因缺乏对小鼠心脏重量与体重比值(HW/BW)和心肌细胞大小并没有显著影响(p0.05)。WT+EX组和K0+EX组小鼠HW/BW和心肌细胞横截面积较各自对照组比都显著增大(p0.5),且K0+EX组小鼠HW/BW和心肌细胞横截面积均显著大于WT+EX组(p0.05)。3.AMPK α 2基因缺乏对小鼠心肌纤维化没有显著影响(p0.05),7周跑台训练后未见小鼠出现明显心肌纤维化;WT+Ctr、KO+Ctr、WT+EX和K0+EX各组心肌纤维化水平未见显著性差异(p0.05)。4.与相应的安静对照组相比,7周跑台运动引起WT+EX和KO+EX小鼠的AMPK α总蛋白水平显著提高,(p0.05),KO+EX组AMPK α总蛋白水平显著低于WT+EX组(p0.05),但7周跑台运动后,未见p-AMPKThr172平显著变化(p0.05)。研究结论1.7周跑台运动可引起小鼠心肌肥厚,主要表现为心脏重量增加,心肌细胞横截面积增加。2.7周跑台运动可引起AMPKα总蛋白表达增加,AMPKα2基因缺乏可加重小鼠的运动性心肌肥厚程度。3.7周跑台运动训练并不引起明显的心肌纤维化,AMPK α2基因缺乏对运动性心肌肥厚小鼠的心肌纤维化无显著影响。
[Abstract]:Objective to investigate the role of AMPK 伪 2 in the exercise of AMPK 伪 2 knockout mice and to explore the mechanism of AMPK 伪 2 in exercise induced myocardial hypertrophy. Methods 18 adult male AMPK 伪 2 KOKO mice and 18 wild type control mice were used to study the mechanism of AMPK 伪 2 in exercise induced myocardial hypertrophy. The rats were randomly divided into two groups: exercise group (EXX) and control group (WT Ctrn (WTCtrnX) and KO EX(n=12).WT X) and KO EX(n=12).WT ex and KO ex to establish a model of exercise myocardial hypertrophy. Cardiac ultrasound was used to detect cardiac function and morphology of mice. Picric acid-sirius red staining was used to detect myocardial fibrosis and WGA staining was used to calculate the size of cardiac myocytes and immunoglobulin imprinting method was used to detect the expression of myocardial related proteins. There was no significant difference in echocardiographic results between WT CtrX Ctr and K0EX groups under basic condition. The EF values of WT ex and K0 ex mice were higher than those of control group after running on the platform for 7 weeks. But there was no significant difference between WT EX and KO EX groups. Compared with the control group, there was a significant increase in the left ventricular wall thickness (VPWS) in the WT EX group and KO ex group compared with the control group. The left ventricular end-systolic wall thickness (VPWS) in the WT EX group was significantly higher than that in the WT Ctr group, and the left ventricular end-systolic wall thickness (VPWS) in the Ko EX group was significantly higher than that in the WT Ctr group. The lack of AMPK 伪 2 gene had no significant effect on the ratio of heart weight to body weight and the size of cardiomyocytes in mice in quiet state. The cross sectional area of HW/BW and cardiomyocytes in WT ex group and K0 ex group were significantly higher than those in control group. The cross sectional area of HW/BW and cardiomyocytes in K0 ex group was significantly larger than that in WT ex group. 3. The absence of AMPK 伪 2 gene had no significant effect on myocardial fibrosis in mice. There was no significant difference in myocardial fibrosis level between WT ex and K0 ex groups. Compared with the quiet control group, the total protein level of AMPK 伪 in WT ex and KO ex mice induced by 7 weeks treadmill exercise was significantly increased. The average level was significantly lower than that in WT ex group (P 0.05), but after 7 weeks of treadmill exercise, No significant change of p-AMPKThr172 level was observed. Conclusion 1.7-week treadmill exercise can induce myocardial hypertrophy in mice, which is mainly manifested by increased heart weight. Increased cross-sectional area of cardiomyocytes. 2.7 weeks of treadmill exercise can increase the expression of AMPK 伪 total protein. The lack of AMPK 伪 2 gene can aggravate the degree of exercise myocardial hypertrophy in mice. 3.7-week treadmill exercise training does not cause obvious myocardial fibrosis and AMPK 伪 2 group. There was no significant effect on myocardial fibrosis due to lack of exercise myocardial hypertrophy in mice.
【学位授予单位】：上海体育学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：G804.7

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