Department of Experimental Medicine, Pharmacology Division, University of Campania "L. Vanvitelli", 80138, Naples, Italy.
Department of Precision Medicine, University of Campania "L. Vanvitelli", 80138, Naples, Italy.
Life Sci. 2019 Apr 1;222:140-147. doi: 10.1016/j.lfs.2019.03.001. Epub 2019 Mar 5.
To investigate the cardioprotective effects of prolonged and moderate exercise training on cellular and molecular events early after myocardial infarction.
Male Wistar rats were divided in sedentary or exercised group; both groups underwent to a myocardial infarction. All the molecular and immunohistochemical analyses on hearts of sedentary and exercised rats were performed 48 h after surgical procedure. SIRT1 and SIRT3 expression were measured and two of the pathways activated by sirtuins, p53-induced apoptosis and Forkhead boxO (FOXO)3a-induced oxidative stress, were investigated. All the experiments were performed also in presence of the SIRT inhibitor, EX527.
Fourty-eight hours post myocardial infarction, exercise training induced the activation of SIRT1 and SIRT3 pathway reducing cardiomyocytes apoptosis and oxidative damage. Molecular data were confirmed by immunohistochemical evaluations. These effects are more evident in border infarcted zone than in the remote myocardium.
Exercise training is a non-pharmacological prevention strategy in cardiovascular diseases and the sirtuins family seems to be as novel and attractive target in cardioprotection.
研究长期适度运动训练对心肌梗死后早期细胞和分子事件的心脏保护作用。
雄性 Wistar 大鼠分为安静组和运动组;两组均进行心肌梗死。所有分子和免疫组化分析均在手术 48 小时后进行。测量 SIRT1 和 SIRT3 的表达,并研究 Sirtuins 激活的两条途径,p53 诱导的细胞凋亡和 Forkhead boxO(FOXO)3a 诱导的氧化应激。所有实验均在 SIRT 抑制剂 EX527 的存在下进行。
心肌梗死后 48 小时,运动训练诱导 SIRT1 和 SIRT3 通路的激活,减少心肌细胞凋亡和氧化损伤。分子数据得到免疫组化评估的证实。这些作用在梗死周边区比在远隔心肌更为明显。
运动训练是心血管疾病的一种非药物预防策略,而 Sirtuins 家族似乎是心脏保护的一个新颖而有吸引力的靶点。