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Objective:Myocardial ischemia/reperfusion(I/R) injury is the leading cause of death in the world. However,the details of the mechanism of its pathophysiology are still unknown. The present study was designed to investigate the role of connexin 43(Cx43) in acute models of myocardial I/R injury. Methods:Male C57BL/6 mice were subjected to myocardial ischemia(45 min) followed by reperfusion(4 hrs) in vivo. The whole operation was monitored using a two-lead ECG. Hearts were harvested and the level of protein was assessed by western blot analysis. Haematoxylin and Eosin(HE) staining was used to detect the extent of neutrophil infiltration. The expression level of IL-6 was detected by ELISA. Results:A murine myocardial I/R injury model was constructed successfully. Phosphorylated Cx43 decreased 83. 45% while non-phosphorylated Cx43 increased 1.62-fold in the myocardium after I/R injury. Neutrophil infiltration and the expression of the inflammatory cytokine IL-6 increased in the myocardium following I/R. Conclusion:During myocardial I/R injury,cardiomyocyte Cx43 is dephosphorylated,and this may be associated with an inflammatory response.
Objective: Myocardial ischemia / reperfusion (I / R) injury is the leading cause of death in the world. However, the details of the mechanism of its pathophysiology are still unknown. The present study was designed to investigate the role of connexin 43 (Cx43 ) in acute models of myocardial I / R injury. Methods: Male C57BL / 6 mice were subjected to myocardial ischemia (45 min) followed by reperfusion (4 hrs) in vivo. The whole operation was monitored using a two- were harvested and the level of protein was assessed by western blot analysis. Haematoxylin and Eosin (HE) staining was used to detect the extent of neutrophil infiltration. The expression level of IL-6 was detected by ELISA. Results: A murine myocardial I / R injury model was constructed successfully. Phosphorylated Cx43 decreased 83. 45% while non-phosphorylated Cx43 increased 1.62-fold in the myocardium after I / R injury. Neutrophil infiltration and the expression of the inflammatory cytokine IL-6 increased in the myocardium f ollowing I / R. Conclusion: During myocardial I / R injury, cardiomyocyte Cx43 is dephosphorylated, and this may be associated with an inflammatory response.