Interleukin-33 prevents high glucose-induced apoptosis in H9c2 cardiac cells by inhibiting reaction oxygen species-activated JNK and p38 MAPK pathway

Interleukin-33 (IL-33), a new member of IL-1 family, has been shown protective effects on many cardiovascular diseases. The present study was to investigate the protective effects of IL-33 against high glucose (HG)induced apoptosis in H9c2 cardiac cells and explore the potential mechanisms. H9c2 cardiac cells were exposed to HG with or without IL-33 pre-treatment. Cell viability was assessed by methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis was detected by flow cytometry. Reactive oxygen species (ROS) was assessed by measuring 2',7'-dichlorodi-hydrofluorescein diacetate (DCFH-DA) oxidation. The protein expressions of cleaved (c)-caspase-3, phosphor (p)-JNK and p-p38 MAPK were determined by Western blotting. Exposure of cells to HG resulted in a loss in cell viability and an increase in apoptosis. HG induced ROS production and phosphorylation of JNK and p38 MAPK. Treatment with IL-33 attenuated HG -induced oxidative stress, prevented JNK and p38 MAPK phosphorylation and attenuated cell apoptosis. Our study demonstrates that IL-33 prevents HG-induced H9c2 cardiac cell apoptosis by attenuating ROS formation and inhibiting the activation of JNK and p38 MAPK.