Abstract
Our previous study demonstrated that hyperbaric oxygen (HBO) preconditioning protected against myocardial ischemia reperfusion injury (MIRI) and improved myocardial infarction. However, HBO’s effect on MIRI-induced inflammation and autophagy remains unclear. In this study, we investigate the potential impact and underlying mechanism of HBO preconditioning on an MIRI-induced inflammatory response and autophagy using a ligation of the left anterior descending (LAD) coronary artery rat model. Our results showed that HBO restored myocardial enzyme levels and decreased the apoptosis of cardiomyocytes, which were induced by MIRI. Moreover, HBO significantly suppressed MIRI-induced inflammatory cytokines. This effect was associated with the inhibition of the TLR4-nuclear factor kappa-B (NF-κB) pathway. Interestingly, lower expression levels of microtubule-associated protein 1 light chain 3B (LC3B) and Beclin-1 were observed in the HBO-treatment group. Furthermore, we observed that HBO reduced excessive autophagy by activating the mammalian target of the rapamycin (mTOR) pathway, as evidenced by higher expression levels of threonine protein kinase (Akt) and phosphorylated-mTOR. In conclusion, HBO protected cardiomocytes during MIRI by attenuating inflammation and autophagy. Our results provide a new mechanistic insight into the cardioprotective role of HBO against MIRI.
Highlights
According to data from 2016, there were approximately 660,000 new myocardial infarction (MI) cases and 305,000 recurrent attacks [1]
Our results showed that hyperbaric oxygen (HBO) restored myocardial enzyme levels and decreased the apoptosis of cardiomyocytes, which were induced by myocardial ischemia reperfusion injury (MIRI)
To evaluate the protective effect of HBO against MIRI, we measured the levels of cardiac troponin I, cardiac troponin T and myoglbin (Mb) in serum at 60 min after reperfusion
Summary
According to data from 2016, there were approximately 660,000 new myocardial infarction (MI) cases and 305,000 recurrent attacks [1]. Autophagy is a critical factor in the heart during MIRI [3,4,5]. It is an evolutionarily conserved lysosomedependent degradation process that plays an essential role in cellular homoeostasis and maintaining instances of nutrient starvation [6, 7]. Current research reports that autophagy plays a dual role in MIRI, involving a slight induction during ischemia to promote cell survival and a sharp increase during reperfusion, triggering myocardial cell death [8, 9]. Threonine protein kinase (Akt), known as serine, is a multifunctional adaptor protein that serves several signaling pathways, including the mTOR-mediated autophagy process, nuclear factor kappa-B (NF-κB), and apoptosis [14]. It is of increasing interest to restore impaired autophagy by these two pathways to alleviate MIRI
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