Resveratrol attenuates high glucose-induced cardiomyocytes injury via interfering ROS-MAPK-NF-κB signaling pathway.

Cardiomyocyte inflammatory injury is likely required for cardiomyocytes death under hyperglycemia condition. Resveratrol (Res) is famous for its anti-inflammatory effect. However, there are few reports about the anti-inflammatory effect of Res induced by high glucose in cardiomyocytes. The aim of the present study is to investigate the inflammatory effect of high glucose and the anti-inflammatory effect of Res induced by high glucose in cardiomyocytes. Primary cardiomyocytes were isolated from new born SD rats and high glucose (30 mmol/L) was used as a stimulant for cell injury. Cell viability was assayed by CCK-8 method; protein expression was identified by Western blot or ELISA, respectively. The production of reactive oxygen species (ROS) was observed under a fluorescence microscope. The results indicated that High glucose (30 mmol/L) significantly decreased the cell viability of cardiomyocytes after co-cultivated for 12 h and had a time-dependent manner, and increased IL-1β, IL-6 and TNF-α secretion in cardiomyocytes. The injury effect of high glucose involved in ROS-MAPK-NF-κB signaling pathway. For the reason that antioxidant NAC, ERK1/2, p38 MAPK and NF-κB specific pathway inhibitors was able to abolish the secretion of this inflammatory factors; pretreatment with antioxidant NAC significantly decreased the level of phosphorylated ERK1/2, p38 MAPK and nuclear NF-κB; pretreatment of PD98059 and SB203580 can significantly decrease NF-κB level in nuclei. After treatment with Res 20 μmol/L for 12 h, IL-1β, IL-6 and TNF-α secretion were markedly decreased, and the phosphorylation of ERK1/2, p38 MAPK and NF-κB level were also decreased. All the results showed that Res attenuates high glucose-induced inflammatory injury through ROS-ERK1/2/p38-NF-κB signaling pathway in cardiomyocytes.