Exercise training combined with alprostadil improves myocardial infarction and coronary microcirculation disorder in aged rats by inhibiting mitogen-activated protein kinase (MAPK) signaling pathway activation.

Abstract

We aimed to explore the effects and mechanisms of exercise training combined with alprostadil (ALPR) treatment on myocardial infarction (MI) in aged rats. Male Wistar rats were randomly divided into five groups. One day after MI induction, an automatic biochemical analyzer was used to measure cardiac troponin I (cTnI), cardiac troponin T (cTnT), and creatine kinase MB isoenzyme (CK-MB) serum levels. One week after MI induction, echocardiography was performed to examine the left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular ejection fraction (LVEF), and left ventricular fraction shortening (LVFS) rates of the rats. Parameters such as body weight (BW), heart mass index, and the heart weight (HW)/tibia length (TL) ratio of the rats were also calculated. Western blot was performed to assess angiogenesis and mitogen-activated protein kinase (MAPK) signal-related protein expression. Compared with the MI group, the LVEDD and LVESD in the Trained + ALPR group were significantly decreased, while LVEF, LVFS, HW/BW, and HW/TL were significantly increased. Additionally, the Trained + ALPR group exhibited decreased levels of cTnI, cTnT, and CK-MB and significantly reduced MI size and myocardial injury. Moreover, compared with the Trained or ALPR group, the Trained + ALPR group showed upregulated energy metabolism, increased microvessel density, and better efficacy. Finally, the Trained + ALPR group showed a significant increase in angiogenesis-related proteins and a significant reduction in MAPK signaling pathway-related protein activity. Exercise training combined with ALPR improved MI in elderly rats by inhibiting MAPK signaling, promoting angiogenesis, and increasing metabolism.