Curcumin protects H9c2 cardiomyocyte against ischemia/reperfusion injury through inactivation of glycogen synthase kinase-3

Curcumin, a polyphenolic compound derived from turmeric, has a protective potential on cardiovascular system. Glycogen synthase kinase-3 (GSK-3) is a multifunctional serine/threonine kinase, which has been demonstrated to play a role in cardioprotection. The present study was aimed to determine the effect of curcumin against ischemia/reperfusion (I/R) injury in cardiomyocyte and its underlying mechanisms involving the role of GSK-3. In this study, an in vitro I/R model was simulated in H9c2 cardiomyocytes. The cell viability, release of lactate dehydrogenase (LDH), cell apoptosis and mitochondrial membrane potential (MMP) were examined in the culture of H9c2 cardiomyocytes following I/R injury. The levels of GSK-3 expression and it’s phosphorylation of tyrosine and serine were also evaluated by Western blotting analysis. The results showed that curcumin increased the cell viability, and decreased the release of LDH and cell apoptosis in the culture of H9c2 cells exposed to I/R. Furthermore, curcumin treatment significantly suppressed the loss of MMP in cardimyocytes exposed to I/R. In addition, I/R injury markedly increased both the activated and inactivated phosphorylation of GSK-3 in H9c2 cells. Curcumin significantly reduced the activated phosphorylations of GSK-3 at tyrosine residues and increased the inactivated phosphorylations of GSK-3 at serine residues. Our findings indicate that curcumin has protective effect against I/R injury in cardiomyocyte, which may partly be mediated by the inactivation of GSK-3 via promoting phosphorylations at serine residues and dephosphorylations at tyrosine residues.