Exercise training enhanced cardiac SIRT1 expression and protected aging induced heart damage in natural aging rats

• Main Authors: Chao-Hung Lai, 賴昭宏
• Other Authors: 黃志揚
• Format: Others
• Language: en_US
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/5qk68t

博士 === 中國醫藥大學 === 老化醫學博士學位學程 === 102 === According to the survey data of the Department of Health, Executive Yuan, ROC (Taiwan) in 101 years, it shows that cardiovascular disease has been in the second (9.1%) of the highest in the top ten leading causes of death, when coupled with related cardiovascular disease and its complications, such as cerebrovascular disease in the thrid (9.3%) and hypertension in the tenth (1.3%). Aging is an immutable law. The function of the heart is in the rate of 1% aging per year. With the advent of the aging society, we must study the serious problem of cardiovascular disease. The demonstrated roles of SIRT1, the mammalian counterpart of the yeast SIR2, reveal that SIRT1 regulates important cellular processes including anti-apoptosis, neuronal protection, cellular senescence, aging and longevity. In the previous studies in obesity in the laboratory, mice with high blood pressure and diabetes slowed down the performance of myocardial apoptosis through sports training. Therefore, this study designed a set of experiments with rats, aging and exercise, to obtain detail discussion of myocardial cells signaling transduction pathway changed. Three groups of different ages, 3 months, 12 months and 18 months old ages of mice were randomly divided into the aging groups (C3, A12 and A18) and exercise groups (E3, AE12 and AE18). Exercise training of swimming five times a week gradual increases from the first week of every 20 min to every 60 min for 12 weeks. Finally, after the complete of the sports training process, we used tissue sections to observe the type of organization (H & E stain), as well as the test of apoptosis (TUNEL Assays) and Western blotting to observe changes in the myocardial tissue and protein. Experimental results show that protein expression of cardiac myocyte apoptotic pathway increased in the aging groups (C3, A12 and A18), while the improvement in the exercise group. In the aging groups (C3, A12 and A18), the expression of the protein in the survival pathway increased with age to reduced performance, but in the exercise groups (E3, AE12 and AE18) increase access to improve performance. In addition, we did a preliminary study of myocardial apoptosis upstream SIRT regulation and the performance of the aging groups (C3, A12 and A18) was not obvious and On the contrary, there was much performance in the exercise groups (E3, AE12 and AE18) and it meant compensatory mechanism. On the other hand, we also obtain that aging induced cardiac fibrosis (C3, A12 and A18), via FGF2 / uPA / MMP2 pathway TGFβ1 / CTGF pathway and concentric cardiac hypertrophy via JNK / ERK1/2 / NFATc3 / GATA4 pathway to enhance cardiac injury, and exercise training (E3, AE12 and AE18) can reverse aging-induced cardiac injury. Therefore, we hope that a more in-depth study by our results of this study to investigate the mechanism of aging-induced heart injury.