Potential of Low Energy UltraSound for Inducing Cardioprotection Mechanisms: In-Vitro Investigations on a Hypoxia-Reoxygenation Model of Cardiac Cells

摘要

In the context of acute myocardial infarction, we propose that Low Energy Ultrasound (LEUS) exposures might attenuate the detrimental effects of ischemia and reperfusion injury. Specifically, our goal is to quantify and monitor the effects of ultrasound using an in vitro cardiac cell model of ischemia-reperfusion. The study was conducted using a mono-layer cell model (H9C2 cardiomyoblasts) exposed to a prolonged hypoxia-reoxygenation (HR) challenge. Two groups were formed: i). HR: cells submitted to hypoxia followed by reoxygenation period, and ii). HR+PostCond-LEUS: LEUS applied repeatedly for 20 min starting at the onset of reoxygenation. Cell death was evaluated by flow cytometry for each group at the end of US exposure. Cell viability was clearly improved in the HR+PostCond-LEUS group, at all time points during reoxygenation. This study suggests a potential protective effect of LEUS on cardiomyoblasts exposed to a prolonged hypoxia-reoxygenation insult. More complex in vitro models exploring potential protective mechanisms (SAFE and RISK signaling pathways and in vivo models will be required for a better comprehension of the underlying mechanisms.