LAUSR

ObjectivesTo investigate the potential role and underlying mechanism of Sirtuin2 (SIRT2) in regulating high glucose (HG)-induced vascular endothelial cell injury by using human umbilical vein endothelial cells (HUVECs).ResultsSIRT2 mRNA and protein expression levels were decreased in HG-treated HUVECs. SIRT2 overexpression increased viability, decreased apoptosis and reduced levels of reactive oxygen species in HG-treated HUVECs. SIRT2 overexpression decreased TNF-α expression (146.5 ± 22.8 pg TNF-α ml−1) relative to that in the empty vector group (263.5 ± 18.5 pg TNF-α ml−1) and decreased MCP-1 expression (63.8 ± 9.85 pg MCP-1 ml−1) relative to that in the empty vector group (105.8 ± 8.5 pg MCP-1 ml−1). SIRT2 overexpression decreased the acetylation of p53 by 33% and decreased the acetylation of NF-κB p65 by 58% in HG-treated HUVECs.ConclusionSIRT2 prevents HG-induced vascular endothelial cell injury through suppressing the p53 and NF-κB signaling pathways.