Curcumin attenuates high glucose-induced inflammatory injury through the reactive oxygen species-phosphoinositide 3-kinase/protein kinase B-nuclear factor-κB signaling pathway in rat thoracic aorta endothelial cells.
Objective: Endothelial cell inflammatory injury is likely required for barrier dysfunction under hyperglycemic conditions. Curcumin (CUR) is well known for its anti-inflammatory effect. However, there have been few reports about the anti-inflammatory effect of CUR induced by high glucose in endothelial cells. The aim of the present study was to investigate the inflammatory effect of high glucose and the anti-inflammatory effect of CUR induced by high glucose in rat thoracic aorta endothelial cells (TAECs).
Methods: Well characterized TAECs were established and cell viability was assayed by the cell counting kit-8 method, messenger ribonucleic acid and protein expression were identified by real-time polymerase chain reaction, western blot or enzyme-linked immunosorbent assay, respectively. The production of reactive oxygen species was observed by a fluorescence microscope.
Results: High glucose (30 mmol/L) significantly decreased the cell viability of TAECs after being co-cultivated for 12 h and showed a time-dependent manner, and increased interleukin (IL)-1β, IL-6 and tumor necrosis factor-α secretion in TAECs. The injury effect of high glucose was involved in the reactive oxygen species-phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)-nuclear factor (NF)-κB signaling pathway. Anti-oxidant N-acetylcysteine, PI3K and NF-κB-specific pathway inhibitors can abolish the secretion of these inflammatory factors; pretreatment with anti-oxidant N-acetylcysteine significantly decreased PI3K expression, the level of phosphorylated AKT and nuclear NF-κB; pretreatment of LY294002 can significantly decrease the NF-κB level in nuclei. After treatment with CUR for 12 h, IL-1β, IL-6 and tumor necrosis factor-α secretion were markedly decreased, and PI3K expression, the phosphorylation of AKT and nuclear NF-κB level were also decreased.
Conclusions: Curcumin attenuates high glucose-induced inflammatory injury through the reactive oxygen species-PI3K/AKT-NF-κB signaling pathway in rat thoracic aorta endothelial cells.