Mild hypothermia (35°C) reduces myocardial ischemia-reperfusion injury and attenuates hypoxia induced apoptosis of H9C2 cardiomyocytes by changing the phosphorylation level of Connexin43 (Cx43) protein.

BACKGROUND: The purpose of this study was to investigate the effect of connexin 43 (Cx43) on myocardial cell apoptosis under mild hypothermia and its potential for treating ischemia reperfusion injury. METHODOLOGY: In vivo experiments were conducted on rats, using an ischemia-reperfusion model, small animal ultrasound imaging system, and relevant biochemical assays to measure myocardial function, infarction area, and tissue damage. In vitro experiments were performed on H9C2 cells using an oxygen-glucose deprivation and recovery model, and various assays were used to assess cell viability, apoptosis, and biochemical changes. RESULTS: Mild hypothermia (35°C) was found to reduce ischemia-reperfusion injury, enhance myocardial function, decrease infarction area, and increase the expression of phosphorylated Cx43 and protein kinase C in myocardial tissue. In vitro, mild hypothermia enhanced cell viability, decreased gap junction permeability, downregulated pro-apoptotic factors, and upregulated anti-apoptotic factors, while also increasing the levels of calcium and superoxide dismutase and decreasing the level of malondialdehyde. CONCLUSIONS: Mild hypothermia can protect against myocardial ischemia-reperfusion injury by regulating the level of phosphorylated Cx43 protein, which reduces myocardial cell apoptosis and enhances cardiac function. This study highlights the potential therapeutic benefits of mild hypothermia in treating ischemia-reperfusion injury.