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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.
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Objective To investigate the effect of PPARγ in acute coronary syndrome (ACS) patients with type 2 diabetes (T2DM) for the severity of coronary atherosclerosis and plaque stability. Methods We selected 102 patients with ACS, including 52 patients with type 2 diabetes mellitus (ACS+T2DM group) and 50 patients with simply ACS (ACS group). Meanwhile, we selected 30 patients without coronary heart disease and T2DM as the control group. All basic clinic data, CAG and the Gensini score were compared among all groups. To all patients, blood was drew when they were enrolled to detect the level of PPARγ and MMP-9. Results Gensini points in the ACS+T2DM group was much higher than that of the ACS group (P < 0.05). The levels of PPARγ of the ACS group and the ACS+T2DM group, when compared with the control group, were decreased significantly, but the level of MMP-9 were increased (all P < 0.05). The level of PPARγ in the ACS+T2DM group was much lower than the ACS group, and the level of MMP-9 was much higher (P<0.05). Gensini scores (r=-0.416, P<0.05), the level of MMP-9(r= - 0.503, P < 0.05) were correlated negatively with the level of PPARγ. Conclusions Complicating with T2DM can aggravate coronary artery disease and plaque instability degree in ACS patients, and PPARγpossibly make an protective effect.