Sulfur dioxide restores calcium homeostasis disturbance in rat with isoproterenol-induced myocardial injury

Abstract

Backgrounds: sulfur dioxide (SO2) could relieve isoproterenol (ISO)-induced myocardial injury, while the mechanism is unclear. This study aims to explore whether the protective effect of SO2 on ISO-induced myocardial injury was mediated by the restoration of calcium homeostasis disturbance in cardiomyocyte. Methods and results: Rats were randomly divided into four groups: ISO group, ISO+SO2 group, control group and SO2 group. Content of Ca2+ in H9c2 cells was assayed using confocal microscope, and cardiac function parameters were measured by echocardiography. Plasma biochemical values and myocardial ultra-structure changes were measured. Meanwhile, the activity, protein and gene levels of sarcoplasmic reticulum Ca2+ ATPase (SERCA), and protein and phosphorylation of phospholamban (PLN) were detected. We found SO2 derivatives could restore the decreased cardiac function, the abnormal lactate dehydrogenase, creatine kinase, alpha-hydroxybutyrate dehydrogenase, potassium, calcium, blood urea nitrogen and the damaged myocardial ultra-structure in rats, and regulate the increased Ca2+ content in H9c2 induced by ISO. In addition, compared with ISO group, the decreased activities, protein and mRNA level of SERCA, as well as the decreased protein phosphorylation level of PLN in myocardial tissues were increased in ISO+SO2 group. Conclusion: SO2 derivatives might relieve calcium overload in association with the upregulating expression of SERCA and p-PLN/PLN by myocardial tissues in rats with ISO-induced myocardial injury