Nicorandil alleviates inflammation and oxidation in diabetic cardiomyopathy

Purpose: To examine the effect of nicorandil on high glucose-induced cardiomyocyte inflammation and oxidative stress. Methods: H9C2 cardiomyocytes were divided into control group, high glucose group and nicorandil group. The survival rate of cardiomyocytes was determined using the CCK-8 method. The contents of reactive oxygen species (ROS) of cardiomyocytes were determined by flow cytometry. The contents of MDA and LDH in cell supernatant were determined by kit. Western blot and real-time PCR were used to assess oxidative stress, inflammation and apoptosis related factors in each group of cardiomyocytes. The expression levels of IL-1 beta were determined by immunofluorescence. Tunnel staining was used to determine the apoptosis level of each group. Results: The expressions of SOD1 and SOD2 in the high glucose group were significantly decreased (p < 0.05). Also, the contents of MDA and LDH were significantly increased (p < 0.05). Furthermore, IL-1 beta, TNF-alpha, caspase 3 and Bax expressions were increased, while Bcl-2 expression was inhibited. IL-1 beta and Tunnel fluorescence also increased significantly. NF-kappa B and Ikk alpha were significantly increased, while I kappa B-alpha was inhibited. Furthermore, nicorandil inhibited oxidative stress and apoptosis, as well as NF-kappa B pathway and downstream factor Ikk alpha. Conclusion: Nicorandil ameliorates the inflammation and oxidative damage of cardiomyocytes induced by high glucose, by inhibiting NF-kappa B pathway, thereby lowering apoptosis. Thus, the findings provide new insight into the development of new agents for the treatment of diabetic cardiomyopathy.