Open AccessCurcumin 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
Author(s) -
Zhang Zhen,
Li Keming
Publication year - 2018
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/jdi.12767
Subject(s) - viability assay , pi3k/akt/mtor pathway , protein kinase b , reactive oxygen species , ly294002 , tumor necrosis factor alpha , curcumin , medicine , proinflammatory cytokine , protein kinase a , kinase , pharmacology , signal transduction , inflammation , biochemistry , chemistry , apoptosis
Aims/Introduction 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 ( TAEC s). Materials and Methods Well characterized TAEC s 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 TAEC s 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 TAEC s. The injury effect of high glucose was involved in the reactive oxygen species–phosphoinositide 3‐kinase ( PI 3K)/protein kinase B ( AKT )–nuclear factor ( NF )‐κB signaling pathway. Anti‐oxidant N‐acetylcysteine, PI 3K and NF ‐κB‐specific pathway inhibitors can abolish the secretion of these inflammatory factors; pretreatment with anti‐oxidant N‐acetylcysteine significantly decreased PI 3K expression, the level of phosphorylated AKT and nuclear NF ‐κB; pretreatment of LY 294002 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 PI 3K expression, the phosphorylation of AKT and nuclear NF ‐κB level were also decreased. Conclusion Curcumin attenuates high glucose‐induced inflammatory injury through the reactive oxygen species– PI 3K/ AKT – NF ‐κB signaling pathway in rat thoracic aorta endothelial cells.