Interaction between ROS and MAPK pathway mediates high glucose-induced injury in H9c2 cardiac cells

Objective To explore the role of interaction between reactive oxygen species(ROS) and mitogen-activated protein kinase(MAPK) pathway in high glucose(HG)-induced injury in H9c2 cardiac cells.Methods Cell viability was measured by cell counter kit(CCK-8);The changes in morphology and amount of apoptotic cells were tested by Hoechst nuclear staining.The level of intracellular ROS was detected by DCFH-DA staining and photofluorography.The expression level of MAPK protein was tested by Western blot assay.Results Exposure of H9c2 cells to HG(35 mmol / L glucose) for 24 h induced significant injuries,as evidenced by a decrease in cell viability,increases in apoptotic cell amount and ROS production.On the other hand,HG markedly upregulated phosphorylated(p) p38MAPK,p-extracellular signal-regulated protein kinase 1 / 2(ERK1 / 2) and c-Jun Nterminal kinase(JNK)(three members of MAPK) expression level.N-acetyl-cystein(NAC,a ROS scavenger) inhibited HG-induced cytotoxicity and cell apoptosis as well as upregulation of p-p38MAPK,p-ERK1 / 2 and p-JNK expression.Furthermore,the selective inhibitors of p38MAPK,ERK1 / 2 and JNK reduced not only HG-induced cardiomyocyte injury,but also overproduction of ROS.Conclusion During H9c2 cells injury induced by HG,there is a positive interaction between ROS and MAPK pathway.This interaction may play an important role in HG-induced injury in H9c2 cells.