Abstract
Non-invasive positive-pressure ventilation (NIPPV) has been demonstrated to exhibit a cardioprotective function in a rat model of myocardial infarction (MI). However, the mechanism underlying NIPPV-mediated MI progression requires further investigation. We aimed to investigate the effectiveness and corresponding mechanism of NIPPV in an acute MI-induced heart failure (HF) rat model. Thirty each of healthy wild type (WT) and apoptosis signal-regulating kinase 1 (ASK-1)-deficient rats were enrolled in this study. MI models were established via anterior descending branch ligation of the left coronary artery. The corresponding data indicated that NIPPV treatment reduced the heart infarct area, myocardial fibrosis degree, and cardiac function loss in MI rats, and ameliorated apoptosis and reactive oxygen species (ROS) levels in the heart tissue. Furthermore, the expression level of ASK-1 level, a key modulator of the ROS-induced extrinsic apoptosis pathway, was upregulated in the heart tissues of MI rats, but decreased after NIPPV treatment. Meanwhile, the downstream cleavage of caspase-3, caspase-9, and PARP, alongside p38 phosphorylation and FasL expression, exhibited a similar trend to that of ASK-1 expression. The involvement of ASK-1 in NIPPV-treated MI in ASK-1-deficient rats was examined. Although MI modeling indicated that cardiac function loss was alleviated in ASK-1-deficient rats, NIPPV treatment did not confer any clear efficiency in cardiac improvement in ASK-1-knockdown rats with MI modeling. Nonetheless, NIPPV inhibited ROS-induced extrinsic apoptosis in the heart tissues of rats with MI by regulating ASK-1 expression, and subsequently ameliorated cardiac function loss and MI-dependent pathogenic changes in the heart tissue.
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