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Moderate hypothermia plays a major role in myocardial cell death as a result of hypoxia/reoxygenation (H/r) injury. However, few studies have investigated the molecular mechanisms of hypothermic cardioprotection. Several responses to stress and other cell functions are regulated by post-translational protein modifications controlled by small ubiquitin-like modifier (SUMO). Previous studies have established that high SuMoylation of proteins potentiates the ability of cells to withstand hypoxic-ischemic stress. The level to which moderate hypothermia affects SuMoylation is not fully understood, as the functions of SuMoylation in the heart have not been studied in depth. The aim of the present study was to investigate the effect of moderate hypothermia (33˚C) on the protective functions of SuMoylation on myocardial cells. Hl-1 and H9c2 cells were treated with the hypoxia-mimetic chemical cocl 2 and complete medium to simulate H/r injury. Hypothermia intervention was then administered. a cell counting kit-8 assay was used to analyze cell viability. Mitochondrial membrane potential and the generation of reactive oxygen species (roS) were used as functional indexes of mitochondria dysfunction. Bcl-2 and caspase-3 expression levels were analyzed by western blotting. The present results suggested that moderate hypothermia significantly increased SuMo1 and Bcl-2 expression levels, as well as the mitochondrial membrane potential, but significantly decreased the expression levels of caspase-3 and mitochondrial roS. Thus, moderate hypothermia may enhance SuMoylation and attenuate myocardial H/r injury. Moreover, a combination of SuMoylation and moderate hypothermia may be a potential cardiovascular intervention.

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