[SIRT1 signaling pathway mediated the protective effects on myocardium of rats after endurance training and acute...

Objective: To detect the expression of SIRT1 and Ac-FOXO1 in rats after endurance training and acute exhaustive exercise, and explicit the myocardial protective effect of SIRT1. Methods: Rats were randomly divided into four groups: control group(n=20), exhaustive exercise group (E group, n=20), exhaustive exercise group + endurance training (TE group, n=18), exhaustive exercise group + endurance training + selective SIRT1 inhibitor (TSE group, n=17). The Control and E groups were fed routinely for 5 weeks. The TE and TSE groups were subjected to swimming exercise for 5 weeks for endurance exercising. The TSE group was intraperitoneally injected with selective SIRT1 inhibitor Sirtinol(2 mg/kg) at 30 minutes before endurance exercising. The E, TE and TSE groups were subjected to exhaustive exercise. The myocardial tissues of rats were collected after exhaustive exercise. Real-time polymerase chain reaction (PCR) and Western blot analysis were performed to detect the myocardial mRNA and protein expressions of SIRT1 and Ac-FOXO1. The myocardial protein expression of Bax and Bcl-2 was also detected by Western blot. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay was used to assess the apoptosis of myocardial cells. Results: Compared with Control group, the SIRT1 and Bcl-2 expression in the myocardial tissue was obviously decreased, while the Ac-FOXO1, Bax, and the myocardial cell apoptosis were significantly increased in E group (all P<0.01). Compared with E group, the expression of SIRT1 and Bcl-2 was obviously up-regulated (both P<0.01), while the Ac-FOXO, Bax and the myocardial cell apoptosis was significantly reduced in TE group (all P<0.01). Compared with TE group, the SIRT1 and Bcl-2 expression was obviously lower (both P<0.01), while Ac-FOXO1, Bax, and the cell apoptosis were significantly higher in group TSE (all P<0.01). Conclusion: Endurance training could protect myocardium by reducing the myocardial oxidative stress injury and apoptosis via activating SIRT1 signaling pathway, up-regulating the myocardial expression of SIRT1 and regulating the deacetylation of FOXO1.