Wenguang Zhang1, Dongmei Liu2, Jianzhuang Ren1, Pengli Zhou1, Xinwei Han3. 1. Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, East No. 1 Jianshe Road, Zhengzhou, Henan Province, 450052, China. 2. Department of Radiation Oncology, Henan Province Cancer Hospital, Zhengzhou, Henan Province, 450008, China. 3. Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, East No. 1 Jianshe Road, Zhengzhou, Henan Province, 450052, China. han_xinweixw@163.com.
Abstract
OBJECTIVES: To 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). RESULTS: SIRT2 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. CONCLUSION: SIRT2 prevents HG-induced vascular endothelial cell injury through suppressing the p53 and NF-κB signaling pathways.
OBJECTIVES: To 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). RESULTS:SIRT2 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. CONCLUSION:SIRT2 prevents HG-induced vascular endothelial cell injury through suppressing the p53 and NF-κB signaling pathways.